Talk:Alzheimer's disease/Archive 11

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Archive 5 Archive 9 Archive 10 Archive 11 Archive 12


Edit request

I request that the first sentence in the article be changed to say that Alzheimer's disease is not the most common FORM of dementia, but rather the leading CAUSE of dementia, in accordance with this WHO-link:

Please take this into consideration. (talk) 17:51, 11 November 2013 (UTC)

Done Sounds reasonable to me, but someone more knowledgable may undo your change. Thanks, Celestra (talk) 04:20, 13 November 2013 (UTC)

I think that the section genetics (2.1) should be updated with a more exhaustive descriptions of the mutations, why they are pathogenic and proper references from the scientific literature. This will not expand the section too much. Can the section 2.1 genetics be unprotected for me?

--Flick71 (talk) 18:11, 5 December 2013 (UTC)

Please see my reply below at #Alzheimer's Medicines in Development. Maralia (talk) 18:21, 5 December 2013 (UTC)

Merge student project

I've gone through Alzheimer's disease and diet, a student project, to remove some editorializing, prune the primary sources, and leave what can be sourced to reviews. Some of the reviews cited there are at odds with the text in the main article (here). I propose that someone determine what can be merged from the Diet article to here. SandyGeorgia (Talk) 02:10, 19 December 2013 (UTC)

Let me look... Doc James (talk · contribs · email) (if I write on your page reply on mine) 02:43, 19 December 2013 (UTC)
Sigh. Done. Doc James (talk · contribs · email) (if I write on your page reply on mine) 03:24, 19 December 2013 (UTC)

New Articles on the location of start of Alzheimer's

Recently there was an article published in Nature Neuroscience talking about the region of the brain where Alzheimer's starts. From a summary:

It has been known for years that Alzheimer's starts in a brain region known as the entorhinal cortex," said co-senior author Scott A. Small, MD, Boris and Rose Katz Professor of Neurology, professor of radiology, and director of the Alzheimer's Disease Research Center. "But this study is the first to show in living patients that it begins specifically in the lateral entorhinal cortex, or LEC. The LEC is considered to be a gateway to the hippocampus, which plays a key role in the consolidation of long-term memory, among other functions. If the LEC is affected, other aspects of the hippocampus will also be affected."

I believe that this has some relevance for the pathophysiology section, but would really appreciate some comment.

Links: (this is the press release, many other articles use it as their article source)

Thanks,Feynmanistheman (talk) 07:55, 26 December 2013 (UTC)

Per WP:MEDRS we typically use second sources such as review articles rather than primary sources. Doc James (talk · contribs · email) (if I write on your page reply on mine) 23:15, 26 December 2013 (UTC)

Indeed this paper is pertinent to the first, rather vague, sentence under the heading Neuropathology: "Alzheimer's disease is characterised by loss of neurons and synapses in the cerebral cortex and certain subcortical regions." I see my citation has been reverted which is irritating since reporting that the entorhinal cortex is where the neurodegeneration starts is important. The paper has an abstract which seems to me understandable to readers of this article so i see no reason to remove my citation.Richwil (talk) 14:21, 17 January 2014 (UTC)

If it is notable it should be in a secondary source. Doc James (talk · contribs · email) (if I write on your page reply on mine) 14:46, 17 January 2014 (UTC)
Did you observe the notice before you edited? This is a broad, overview, Featured article, which must rely on highest quality sources per FA sourcing standards and medical sourcing guidelines. Giving one primary source prominence, when it hasn't been reviewed by secondary sources, would also be undue. SandyGeorgia (Talk) 14:50, 17 January 2014 (UTC)
  • There are numerous secondary sources to support this (the entorhinal role, not specifically the lateral entorhinal role), for example PMID 21331296. Looie496 (talk) 16:26, 17 January 2014 (UTC)
This article is so out of date probably due to a cabal of editiors frightened to keep pace with research. Issues such as primary progressive aphasia are not even mentioned. dolfrog (talk) 19:05, 17 January 2014 (UTC)

This article seems to be missing information...

...about how many people die annually from Alzheimer's disease, a topic which has been in the news lately because of a new study suggesting that the figure is about 500,000 per year (in 2010) just in the United States. While I am aware this is not a MEDRS compliant source, I still am of the opinion that this topic should be discussed in this article. Jinkinson talk to me 16:07, 6 March 2014 (UTC)

Perhaps this would be a better source. Jinkinson talk to me 16:10, 6 March 2014 (UTC)
Sure that looks good. Doc James (talk · contribs · email) (if I write on your page reply on mine) 20:19, 10 March 2014 (UTC)

And what about inflammation in AD?

The DANA Foundation - A New Look at Brain Inflammation in Alzheimer's: "Since the late 1980s, various studies have found hints that the chronic inflammation found in Alzheimer’s hastens the disease process, and may even be a disease trigger. A history of serious head injury, which typically causes brain inflammation, is known to be a risk factor for Alzheimer’s. Systemic infection—another cause of inflammation—also appears to accelerate the disease. Several epidemiological studies have found that older people who use anti-inflammatory drugs regularly appear to have significantly lower incidences of Alzheimer’s. The value of those epidemiological studies came into question several years ago, when more rigorous placebo-controlled clinical trials of anti-inflammatory drugs—ibuprofen, naproxen, and celecoxib, for example—failed to show signs of helping people who already have Alzheimer’s dementia or early cognitive impairment. In some cases these drugs apparently accelerated the course of the disease. Yet in a little-publicized study, published in late 2011, naproxen seemed to have a marked effect in preventing the disease: It reduced the incidence of Alzheimer’s among elderly people who started out cognitively normal and took the drug for more than two years..." good references: and AlzFighter (talk) 22:03, 20 January 2014 (UTC)

This article [1] does not mention naproxen? Doc James (talk · contribs · email) (if I write on your page reply on mine) 17:09, 11 March 2014 (UTC)
@doc james: It does: page 29, first paragraph, ref 43. please read before you comment. Dimitrije Krstic (talk) 13:58, 17 March 2014 (UTC)
Hi, Dimitrije. I take it you refer to the first paragraph of your own Nature paper there, while DocJames was referring to PMC3750399. In any case, welcome to Wikipedia. We'd love to have you stick around and help build the encyclopedia. If you are so inclined, you'll want to read wp:Why register. While not essential, it does help facilitate collaboration. Cheers, LeadSongDog come howl! 20:37, 17 March 2014 (UTC)
yes, my mistake. appologies to doc james. confusing was ("ref. 1") and I havent check the link. anyway, I was thinking why nobody of wiki editors wants to include inflammation theory of AD in "other theories section". there is so much literature on the topic, my review is just one of many.... I even recall writing a sentence or two a year ago, but nothing happened. dimitrije (talk) 03:21, 21 March 2014 (UTC)

Semi-protected edit request on 25 April 2014

investigational is misspelled in the last paragraph (talk) 20:38, 25 April 2014 (UTC)

Red information icon with gradient background.svg Not done: only because this is a duplicate request with the one below. —KuyaBriBriTalk 21:02, 25 April 2014 (UTC)

Semi-protected edit request on 25 April 2014

investigational is misspelled in the last paragraph (talk) 20:38, 25 April 2014 (UTC)

Yes check.svg Done Minor edit only. —KuyaBriBriTalk 21:04, 25 April 2014 (UTC)

What's wrong with this?

(copied the question below from my talk page, with permission of User:Hans Haase) Jytdog (talk) 13:17, 28 April 2014 (UTC)

[2]? --Hans Haase (talk) 20:36, 26 April 2014 (UTC)

Hi Hans, thanks for your note, but this is better done at the Talk page of the article. May I move your question there, and respond there? thx Jytdog (talk) 20:43, 26 April 2014 (UTC)
Yes, pse. --Hans Haase (talk) 13:14, 28 April 2014 (UTC)
done Jytdog (talk)
OK, to answer, I reverted you in this dif with edit note "looked for review that discussed this; there are none. fails MEDRS". Some more detail now. First of all, this is a Featured Article, so we watch it carefully to make sure that all changes to it comply with all relevant policies and guidelines in the most excellent way possible - this is one of our best articles (and most read) and so it is important that we keep it that way. So, why was your edit less than excellent? If you read WP:MEDRS (and please please do) you will see that for any content that is biomedical or health related - as your edit was - it should be supported by a secondary source - a review in the biomedical literature. The reasons for this are explained in the MEDRS guideline. I looked for a review discussing the content you added and didn't find one - it appears to be too new. Once it appears in a review we can bring this content in. Jytdog (talk) 13:22, 28 April 2014 (UTC)
Tnx, is a better source? : Parra-Damas A, Valero J, Chen M, España J, Martín E, Ferrer I, Rodríguez-Alvarez J, Saura CA (2014). "Crtc1 activates a transcriptional program deregulated at early Alzheimer's disease-related stages". J. Neurosci. 34 (17): 5776–87. PMID 24760838. doi:10.1523/JNEUROSCI.5288-13.2014.  --Hans Haase (talk) 13:54, 28 April 2014 (UTC)
thanks for talking! That is also a primary source. If you read MEDRS, it has a section on definitions - the exact section is here. Generally authors of a review will explicitly say they are doing a review, and indexing services like MEDLINE and pubmed tag reviews as such. here is the query I did at pubmed looking for reviews of Crtc1 and Alzheimers. There are none. If I may ask, why is this important to you? Jytdog (talk) 13:59, 28 April 2014 (UTC)
This is the translated text. As a 2nd src the Deutschlandfunk confirms the production of Crtc1 ist blocked in AD. With mice a success is confirmed by treading with the missing drug, but not even tested on humans. There are "hypothesises" about AD, also about these plaques. Brains with plaques were found but no symptoms of AD until dead of the brains owner. The plaques apear to be more theory of an other cause as the Crtc1. WP:MEDRS I did not know. I followed basicly collecing the knowledge, but I found this one. --Hans Haase (talk) 14:50, 28 April 2014 (UTC)
this will be my last response. Yes the media gets very excited about some scientific publications. Mainstream media is not a secondary source under MEDRS. Please read WP:MEDRS.Jytdog (talk) 15:09, 28 April 2014 (UTC)
PMID: 21476939 --Hans Haase (talk) 16:38, 28 April 2014 (UTC)

──────────────────────────────────────────────────────────────────────────────────────────────────── nice find! a review on CREB signalling in AD. What content would you want to introduce based on that review? Jytdog (talk) 17:18, 28 April 2014 (UTC)

Possible source about smell and vision tests to detect Alzheimers

See here.--Tomwsulcer (talk) 10:36, 13 July 2014 (UTC)

Primary source around which a lot of hype was generated. We don't use things like this. Great analysis of this study and take-down of the hype around it here. Jytdog (talk) 11:44, 13 July 2014 (UTC)
NBC News and BBC are secondary sources, but in your view, you feel that they are unreliable for this story?--Tomwsulcer (talk) 12:29, 13 July 2014 (UTC) Okay, saw the guideline in MEDRS, I see what you mean. Yes, lots of back-and-forth in popular media, saying eat this, don't eat that, and then it changes ten years later; good idea to stick with medical journals.--Tomwsulcer (talk) 12:33, 13 July 2014 (UTC)
 :) Thanks! Jytdog (talk) 12:49, 13 July 2014 (UTC)

IGAP Result Missing from the Article's Genetics section

IGAP (The International Genomics of Alzheimer's Project {The largest GWAS study ever conducted in Alzheimer's disease}) is not mentioned in the article.

"Meta-analysis of 74,046 individuals identifies 11 new susceptibility loci for Alzheimer’s disease". Nat Genet. 45 (12): 1452–1458. 2013 Dec. PMID 24162737.  Check date values in: |date= (help)

This result should be included in the genetics section. Jedit1 (talk) 23:11, 28 June 2014 (UTC)

The results should be included but mentioning the project itself is not really needed. What wording do you suggest? Doc James (talk · contribs · email) (if I write on your page reply on mine) 01:53, 29 June 2014 (UTC)

"A large GWAS study has found that the genes CASS4,CELF1,FERMT2,HLA-DRB5,INPP5D,MEF2C,NME8,PTK2B,SORL1,ZCWPW1,SlC24A4 also contribute to risk for Late Onset AD. Only CD33 did not replicate among the established AD genes."

The last 4 genes listed from recent GWAS ( i.e. ATP5H,EXOC4,CTNNA3, RNF219) in the wiki article are not widely accepted AD genes. These genes did not appear in the mega meta-analysis above, nor do they appear on Alzforum's Alzgene top 10. The Alzforum Alzgene top 10 list are the generally accepted list of AD genes. IGAP verified 9 of them.

A figure showing risk of AD versus frequency would be a great addition to the article. (I am not sure how to upload the file). Jedit1 (talk) 05:11, 29 June 2014 (UTC)

Okay updated. Doc James (talk · contribs · email) (if I write on your page reply on mine) 05:33, 29 June 2014 (UTC)

Apart from ApoE-ε4, IGAP considered CR1, BIN1, CD2AP, EPHA1, CLU, MS4A6A, PICALM, ABCA7,and CD33 to be known GWAS-defined genes for AD. However, CD33 did not replicate in the IGAP study.Jedit1 (talk) 15:17, 29 June 2014 (UTC)

I don't agree that anything from this study should be in WP - while it is a large study, it is still a primary source. here is the most recent review I could find; it discusses findings from GWAS discussed above. Let's use it instead, OK? Jytdog (talk) 15:29, 29 June 2014 (UTC)

The last edit removed the top 10 AD genes! The 10 established AD genes ( CR1,BIN1,...) should be re-added to the article! I am not sure about whether IGAP should be directly cited. The problem with the review articles is that they are only able to say IGAP says this, IGAP says that. None of the current studies have the massive scale that IGAP has. IGAP found 11 new AD genes and replicated the results in the meta-analysis!

I think it would be helpful to add an article in wiki about this new generation of mega GWAS. The genetics research community struggled (largely without success) for at least 20 years to decipher the genetics of illness. During the last year a new generation of massive GWAS has emerged that is revealing an impressive amount of the genetics of complex illnesses. IGAP is one such study. There is also a large psychiatric GWAS study underway for example, in schizophrenia ). Look at page 21 for the exponential increase in number of SNPS that are expected to be found as GWAS size increases. There should be an article on wiki that documents this profound change in the ability of GWAS to unravel the complex architecture of many human diseases. Schizophrenia until recently was widely considered an undicipherable illness. However, the above url page 21, notes that GWAS studies of 100,000 to 200,000 people would unravel a substantial portion of the genetics of schizophrenia. If this idea were more broadly understood, then there might be political and social pressure exerted to move such GWAS forward, as there would be substantial rewards to finally solving these problems.

Perhaps we could incubate a page for mega GWAS on this talk page and then migrate the page to a wiki article. Jedit1 (talk) 18:55, 29 June 2014 (UTC)

The publication of IGAP is a primary source. Secondary sources are always preferred. And as I mentioned, there is at least one already that discusses IGAP. please see WP:MEDRS.
This appears to be a secondary source [3] Doc James (talk · contribs · email) (if I write on your page reply on mine) 00:25, 30 June 2014 (UTC)
nope - two stages. first stage was new research from old data, and second stage was new research done based on the conclusions from first stage. primary source! big study for sure, but primary source.Jytdog (talk) 02:45, 30 June 2014 (UTC)
It was a "meta-analysis of genome-wide association studies" thus a secondary source. Doc James (talk · contribs · email) (if I write on your page reply on mine) 03:44, 30 June 2014 (UTC)

Text in question

More recent genome-wide association studies (GWAS) have found 19 areas in genes that appear to affect the risk.[1] These genes include: CASS4, CELF1, FERMT2, HLA-DRB5, INPP5D, MEF2C, NME8, PTK2B, SORL1, ZCWPW1, SlC24A4, CLU, PICALM, CR1, BIN1, MS4A, ABCA7, EPHA1, CD2AP,.[1]

Here is the text in question feel free to adjust above and I can add changes. Doc James (talk · contribs · email) (if I write on your page reply on mine) 00:32, 30 June 2014 (UTC)

Apart from ApoE-ε4, IGAP considered CR1, BIN1, CD2AP, EPHA1, CLU, MS4A6A, PICALM, ABCA7,and CD33 to be known GWAS-defined genes for AD. However, CD33 did not replicate in the IGAP study.Jedit1 (talk) 15:17, 29 June 2014 (UTC)
The last edit removed the top 10 AD genes!!!!! The 10 established AD genes ( CR1,BIN1,...) should be re-added to the article! --Jedit1 (talk) 22:22, 30 June 2014 (UTC)

The article might also include reference to synergy in AD. For example, in this article "Synergy between the C2 allele of transferrin and the C282Y allele of the haemochromatosis gene (HFE) as risk factors for developing Alzheimer's disease. J Med Genet.". 41 (4). 2004 Apr: 261–265. PMID 15060098.  Check date values in: |date= (help) all tricarriers (HFE C282Y, TF C2, APOE epsilon 4) developed AD OR=37.5, p<0.0001. Results replicated in 2 subsequent studies "Suggestive synergy between genetic variants in TF and HFE as risk factors for Alzheimer's disease.". Am J Med Genet B Neuropsychiatr Genet. 153B (4): 955–959. 2010 June 5. PMID 20029940.  Check date values in: |date= (help) "Transferrin and HFE genes interact in Alzheimer's disease risk: the Epistasis Project.". Neurobiol Aging. 33 (1): e1–13. 2012 Jan. PMID 20817350.  Check date values in: |date= (help) , though with lower ORs.

However, it is possible that the original results stand within the genetic and environemental context of the original study. Other recent studies have also found extreme AD geno-pheno risk sets (for example, "Risk factors for development of dementia in a unique six-year cohort study. I. An exploratory, pilot study of involvement of the E4 allele of apolipoprotein E, mutations of the hemochromatosis-HFE gene, type 2 diabetes, and stroke.". J Alzheimers Dis. 38 (4): 907–922. PMID 24081379.  Epsilon4 + diabetes, OR=13.5, epsilon4 + stroke, males OR=46.5).

These studies (especially the last) have profound implications for how our societies function. There must be areas in communities with extreme disability. Providing medical services that could reduce the synergistic (that is, multiplicative) increase that occurs from being tri or quad carriers of certain sets of genosets and/or phenosets would likely be a very wise (and cost effective) investment. It is especially relevant to note that the initial tricarriers noted above have a treatable illness (i.e iron overload). Furthermore, these cases of AD would truly be sporadic as such cases would likely not have a family history of AD. In the original study, over 6% of the AD patients had the rare triple combo. The articles noted that over 20% of Western European populations have various mutations in the HFE, TF etc. genes that increase risk of AD.--Jedit1 (talk) 22:22, 30 June 2014 (UTC)

Make a proposal regarding what you want the text changed to in the format:
I want to added "X" supported by ref Y. Doc James (talk · contribs · email) (if I write on your page reply on mine) 22:52, 30 June 2014 (UTC)

It might be better to create an Alzheimer genetics wiki page. Such a page might include a table similar to,_late-onset_%28IGAP%29 . Providing the list of AD genes on the main AD page might not be that helpful. The table could show which mutations have large effect (e.g. APOE epsilon4 , which are rare (e.g. TREM2 p.R47H) etc.) . --Jedit1 (talk) 23:12, 30 June 2014 (UTC)

Sure. Please do. Doc James (talk · contribs · email) (if I write on your page reply on mine) 00:02, 1 July 2014 (UTC)
Jedit1 & Doc James - I haven't read the GWAS cited above, so apologies if I am out of line, but shouldn't the added text say that GWAS "have found 19 areas in genes that appear to correlate to increased risk." rather than "... genes that appear to affect the risk."? Correlation does not equal causation, although the media would often have us believe otherwise. Biolprof (talk) 03:06, 18 July 2014 (UTC)
"appear to affect the risk" sort of means correlation but in simpler language. There is no claim of causation there. Doc James (talk · contribs · email) (if I write on your page reply on mine) 06:18, 18 July 2014 (UTC)

Semi-protected edit request on 4 June 2014

The following text should have "as" added to it. Specifically, it should read "such as the intake of metals".

"Some studies have shown an increased risk of developing AD with environmental factors such the intake of metals, particularly aluminium.[148] The quality of some of these studies has been criticised,[149]"

Since those sources were all quite dated (2008 and older), I went you one better and rewrote the para from a recent review on the (still hot) topic. LeadSongDog come howl! 16:49, 18 July 2014 (UTC)
Addressing the issue of aluminum intake is important as a great deal of alt med literature claims it as a cause but this is not supported by the evidence. Also merged with cause as it was not prevention. Doc James (talk · contribs · email) (if I write on your page reply on mine) 01:28, 19 July 2014 (UTC)

Cannabinoids for treatment of Alzheimer’s disease

This analysis (full text here) from March 2014 might be worth implementing into the main article. Thought I'd just leave this here for you experts who are more familiar with what should and should not go into the articles. — Preceding unsigned comment added by (talk) 06:17, 27 July 2014 (UTC)

Penn State: GABA levels for diagnosing & future treatment target

Was this brought up before? High gamma-aminobutyric acid levels in deformed “reactive astrocytes”. - RoyBoy 23:28, 30 August 2014 (UTC)

Deleted edit

The edit at [4] was deleted, as not MEDRS, but an update is needed. A better choice is likely: which was updated to incorporate guidance in 2011. LeadSongDog come howl! 22:07, 2 September 2014 (UTC)

Yes from my understanding while meds may temporarily help some people with some symptoms none have been shown to delay progression of disease. The benefit with respect to symptoms is controversial. NICE supports a benefit Prescire does not. Doc James (talk · contribs · email) (if I write on your page reply on mine) 04:29, 3 September 2014 (UTC)


I believe the article could elaborate on recent research indicating grey matter atrophy in the brain correlating with cognitive levels in mild-cognitive impairment patients and AD patients.

The article lacks information regarding sever lack of research funding in comparison to other fatal illnesses.

The article fails to mention Alzheimer's being the only cause of death among the top 10 in America without a known way to prevent progression. — Preceding unsigned comment added by Fixler.3 (talkcontribs) 11:07, 1 October 2014 (UTC)

Periodontal disease linkage

Apparently there's a predictive linkage, not just a correlation. No teeth or good teeth *both* show less AD risk than bad teeth, and gingivitis antibodies are found in the brain shortly postmortem.


  • Poole S, Singhrao SK, Crean SJ (2014). "Emerging evidence for associations between periodontitis and the development of Alzheimer’s disease". Faculty Dental Journal. 5 (1): 38–42. 

Primary studies otq:

  • Paganini-Hill A, White SC, Atchison KA (2 AUG 2012). "Dentition, dental health habits, and dementia: the Leisure World cohort study". PMID 22860988. doi:10.1111/j.1532-5415.2012.04064.x.  Check date values in: |date= (help)
  • Stein PS, Steffen MJ, Smith C, Jicha G, Ebersole JL, Abner E, Dawson D (May 2012). "Serum antibodies to periodontal pathogens are a risk factor for Alzheimer’s disease". Alzheimer's & Dementia. 8 (3): 196–203. doi:10.1016/j.jalz.2011.04.006. 
  • Poole S, Singhrao SK, Kesavalu L, Curtis MA, Crean SJ (2013). "Determining the presence of periodontopathic virulence factors in short-term postmortem Alzheimer's disease brain tissue". Journal of Alzheimer's Disease. 36 (4): 665–677. doi:10.3233/JAD-121918. 

I would think that something on this should go with the inflammation discussion. I'm a bit nervous that the reviewers are a bit too close to one of the primary studies, though. Thoughts?LeadSongDog come howl! 18:09, 2 October 2014 (UTC)

Popular press

Agree with this removal [5]. We need to use high quality secondary sources and the content does not belong in the lead. Maybe in a research section. Doc James (talk · contribs · email) (if I write on your page reply on mine) 23:29, 12 October 2014 (UTC)

FWIW - Yes, I *entirely* agree w/ this re related refs[2][3] as well - if interested, some related discussion is here => User talk:Drbogdan#Alzheimer's disease refs - in any case - Enjoy! :) Drbogdan (talk) 12:42, 13 October 2014 (UTC)
  1. ^ a b Lambert, JC (Dec 2013). "Meta-analysis of 74,046 individuals identifies 11 new susceptibility loci for Alzheimer's disease.". Nature genetics. 45 (12): 1452–8. PMID 24162737. 
  2. ^ Choi, Se Hoon et al. (12 October 2014). "A three-dimensional human neural cell culture model of Alzheimer’s disease". Nature (journal). doi:10.1038/nature13800. Retrieved 12 October 2014. 
  3. ^ Kolata, Gina (12 October 2014). "Researchers Replicate Alzheimer’s Brain Cells in a Petri Dish". New York Times. Retrieved 12 October 2014. 

Semi-protected edit request on 18 October 2014

Recently, according to Mayo Clinic, "Tooth loss and gum disease increase the risk of Alzheimer's disease.". So I think that in the "Prevention" section, there should be a subsection that shows that there is an association with tooth loss and gum disease and Alzheimer's disease. 2601:E:100:A00:A0C5:D711:70C0:A765 (talk) 20:14, 18 October 2014 (UTC)

Which ref? Doc James (talk · contribs · email) (if I write on your page reply on mine) 04:36, 19 October 2014 (UTC)

Attention needed to avoid a Featured Article Review


This Featured article was promoted six years ago, and its main author is no longer active on Wikipedia. It has fallen from the status worthy of a Featured article, and has also been subjected to student edits. The article should receive a solid prose and sourcing review, an update, and be generally cleaned up to avoid the need for a Featured article review.

A glaring example is found here:

  • Mental stimulation, exercise, and a balanced diet have been suggested as ways to delay cognitive symptoms (though not brain pathology) in healthy older individuals, but there is no conclusive evidence supporting an effect.[1]
    • First, the source is 2006. A PMID search reviews 2010 and later reviews, that should be/could be used. The conclusion seems to be mostly valid, but someone with better journal access might verify. But worse ...
  • ... when we skip down to the Management section, we find a prominent (undue) link to Music therapy for Alzheimer's disease, leading us to believe music therapy is mainstream proven treatment. That article needs review as well, per MEDRS.

Here are only a couple of examples found on a brief look (there is surely more, and cleaning up these alone may not suffice to retain Featured status according to the criteria):

1a, prose, examples only
  • Alzheimer's disease (AD), also known in medical literature as Alzheimer disease,
    • What does that wording add ? Check throughout for similar prose redundancies.
trimmed. Cas Liber (talk · contribs) 03:29, 22 October 2014 (UTC)
  • It was first described by German psychiatrist and neuropathologist Alois Alzheimer in 1906 and was named after him.
    • Would it not be smoother to combine the clauses to one thought (first described by and named after)?
trimmed. Cas Liber (talk · contribs) 03:29, 22 October 2014 (UTC)
  • although the less-prevalent early-onset Alzheimer's can occur much earlier.
    • Early-onset AZ occurs earlier ... that's helpful.
changed but not deliriously happy with it. Cas Liber (talk · contribs) 10:50, 22 October 2014 (UTC)
  • Although Alzheimer's disease develops differently for every individual, there are many common symptoms.
this sentence is so nebulous as to add nothing to understanding. Removed (sorry OM...) Cas Liber (talk · contribs) 03:43, 22 October 2014 (UTC)
  • Since the disease is different for each individual, predicting how it will affect the person is difficult.
    • That's helpful ... true for most conditions, diseases, etc, and repetitive prose with no useful data or information.
agree - ditched Cas Liber (talk · contribs) 10:50, 22 October 2014 (UTC)
  • Behavior or behaviour ... which version of English is the article using (see WP:ENGVAR).
Let's go British. all intext examples are -our Cas Liber (talk · contribs) 10:54, 22 October 2014 (UTC)
  • often followed by a brain scan if available,
    • What? If available ?
  • AD develops for an unknown and variable amount of time before becoming fully apparent, and it can progress undiagnosed for years.
    • Seems backwards and awkward. AD may be undetected for years would do it.
just ditched it as nebulous Cas Liber (talk · contribs) 10:50, 22 October 2014 (UTC)
  • The cause and progression of the disease are not well understood; it is associated with plaques
    • "It" refers to "cause and progression? Grammatical review needed.
rejigged Cas Liber (talk · contribs) 05:14, 23 October 2014 (UTC)
  • Current treatments only help with the symptoms of the disease.
    • Ugh. Avoid use of current, and doh ... statement says nothing.
rejigged Cas Liber (talk · contribs) 05:14, 23 October 2014 (UTC)
1c, sourcing, samples only, serious update needed

Sources are outdated throughout. (See WP:MEDRS)

  • Alzheimer's is predicted to affect 1 in 85 people globally by 2050.[2]
    • In the first paragraph, we find a statement sourced to 2006 data in a 2007 paper.
  • Fewer than 3% of individuals live more than 14 years after diagnosis.[3]
    • Cited to 1995 data.
2a, lead
  • As of 2012, more than 1,000 clinical trials have been or are being conducted to test various compounds in AD.
    • Why is that in the lead ?

Anyway, this is only a brief list; the article needs to be updated to more recent sources, and to undergo a solid prose review ... the prose is rough and awkward. My other concern is that one can find much better information about AD on other websites, so this does not represent a comprehensive article or Wikipedia's best work.

SandyGeorgia (Talk) 16:15, 19 October 2014 (UTC)

Will try and take a look at this a bit later. Cas Liber (talk · contribs) 20:11, 20 October 2014 (UTC)


  • The information in the "Diet" section is contradicted by this 2014 review: PMID 24925810
  • No mention of this: PMID 25324979
  • Fifteen-year-old paper heavily cited in this article, should be updated:
    • Förstl H, Kurz A. Clinical Features of Alzheimer's Disease. European Archives of Psychiatry and Clinical Neuroscience. 1999;249(6):288–290. doi:10.1007/s004060050101. PMID 10653284.

SandyGeorgia (Talk) 22:04, 20 October 2014 (UTC)

Even more:

  • No discussion of difference between this and vascular dementia.

1 in 85 people

It scared me when the article said "1 in 85 people will get Alzheimer's". Should I keep the "or 82 million people" bit or shall I remove it?

Qwertyxp2000 (talk) 09:05, 17 September 2014 (UTC)

What does the ref say? Doc James (talk · contribs · email) (if I write on your page reply on mine) 11:11, 17 September 2014 (UTC)

"1 in 85 people will get Alzheimer's". Everyone gets Alzheimer pathology. Be scared! The current numbers are 30-40% of people in their mid-80s will develop overt Alzheimer's disease. Of those who do not develop overt AD, many will develop amyloid plaques consistent with AD. Educating people about the ubiquitous incidence of AD pathology might help drive resources to preventing and treating the illness. --Jedit1 (talk) 22:59, 25 October 2014 (UTC)

Sorry this was in the wrong context. 1 in 85 people on the planet currently has AD, though among those in their mid-80s, all will develop AD pathology.--Jedit1 (talk) 23:41, 25 October 2014 (UTC)

Student editing

Hello Alzheimer's page! I am just writing to let any other editors know that this page is being edited within the next few weeks for a class project. We are adding a section to the page on Communication, with subsections that will include information on communication barriers, non-verbal communication techniques, verbal communication techniques, and the affect of cognitive disorders on communication. My group and I would appreciate any feedback you may have on our work. If you would like more information on our project, there is a link posted to our class page on this talk page. Thank-you! Ek13ld (talk) 02:29, 5 November 2014 (UTC)

Please review WP:MEDMOS and WP:OWN#Featured articles and WP:NOTADVICE. This is a featured article and a large number of edits that do not conform with Wikipedia's Medical style guide have been made. Please discuss your edits on talk before making them, and after you have become familiar with medical guidelines for editing. SandyGeorgia (Talk) 15:08, 5 November 2014 (UTC)
Maybe a subpage on the topic? Doc James (talk · contribs · email) 02:04, 7 November 2014 (UTC)
It doesn't appear that suggestions have been taken on board: followup. SandyGeorgia (Talk) 16:52, 20 November 2014 (UTC)
I am the professor for this course. My understanding is that the students heeded advice about refraining from editing this article. They have not made any changes to the article since receiving feedback from editors. They are completing their course assignment in their sandbox and have received peer feedback there. LynnMcCleary (talk) 18:34, 20 November 2014 (UTC)
I am not sure if Sandy's comments are about the article in general - I hate it when we appear unwelcoming at wikipedia but trying to keep (or get) medical articles in acceptable shape is more difficult than many other areas of wikipedia (it is like walking a tightrope), and it is hard to strike a balance between politeness and insistence, which is often needed in these situations. I think it is great that courses are focussing on wikipedia, but I think we might need a way to work more closely with some established editors who work on these type of articles. Cas Liber (talk · contribs) 19:53, 20 November 2014 (UTC)
I concur. I had a very mixed experience of a class project that touched (I don't want to say, "damaged") Distal spinal muscular atrophy type 1. A student's edits required several hours of my work in order to restore the article to a legible state. The "peer review" and "faculty review" made surprisingly little difference. See Talk:Distal spinal muscular atrophy type 1 for discussion; also, the following link shows the changes I and other editors had to make after the class project "improved" the article: For this reason, I would stronglyencourage students to use Sandbox or Talk page to propose any changes before committing them to a live article. Regards, kashmiri TALK 21:20, 20 November 2014 (UTC)
Casliber, I was in fact worried they would drop those edits into this article, so am relieved to hear they won't. And of course it's discouraging that we spend so much time trying to educate student editors, who never return after their term ends, and found that they don't absorb what takes so much of our time. In this article's case, I'm glad our time has been freed up, because the same course is doing same at Hearing loss, where there are reams of off-topic text (I've already moved a lot of it, but I don't have the time to figure out to where to move most of it). SandyGeorgia (Talk) 14:19, 22 November 2014 (UTC)

Section reflist


  1. ^ "More research needed on ways to prevent Alzheimer's, panel finds" (PDF). National Institute on Aging. 29 August 2006. Retrieved 29 February 2008. 
  2. ^ Cite error: The named reference Brookmeyer2007 was invoked but never defined (see the help page).
  3. ^ Cite error: The named reference pmid7793228 was invoked but never defined (see the help page).

Semi-protected edit request on 28 November 2014

In the first paragraph, "As the disease advances" should insert an internal link by instead saying "As the disease advances". 2601:E:100:7C9:5068:8B8F:4ACA:CC83 (talk) 14:44, 28 November 2014 (UTC)

We already link to Neurodegeneration and the two should be merged IMO. Doc James (talk · contribs · email) 14:53, 28 November 2014 (UTC)
Red information icon with gradient background.svg Not done: please establish a consensus for this alteration before using the {{edit semi-protected}} template. Not done on the IPs request and if you think there should be some merging going on, Doc, you'll have to propose that in it's own section below. :) Happy editing! — {{U|Technical 13}} (etc) 16:02, 28 November 2014 (UTC)


Lancet review 2011

  • Ballard, C; Gauthier, S; Corbett, A; Brayne, C; Aarsland, D; Jones, E (19 March 2011). "Alzheimer's disease.". Lancet. 377 (9770): 1019–31. PMID 21371747. 

BMJ 2009

  • Burns, A; Iliffe, S (5 February 2009). "Alzheimer's disease.". BMJ (Clinical research ed.). 338: b158. PMID 19196745. 

NEJM 2010

  • Querfurth, HW; LaFerla, FM (28 January 2010). "Alzheimer's disease.". The New England journal of medicine. 362 (4): 329–44. PMID 20107219. 

Doc James (talk · contribs · email) 08:57, 30 November 2014 (UTC)

Research directions

I just undid the insertion of a new murine study. We've watched a lot of interventions come and go, to the disappointment of many. A few get as far as stage three human trials. Short of that, we don't add them to this article. Alzheimer's disease clinical research can discuss less mature interventions. LeadSongDog come howl! 03:56, 18 December 2014 (UTC)

Yes we need a review. Doc James (talk · contribs · email) 04:56, 18 December 2014 (UTC)

Pathophysiology vs Mechanism

Shouldn't the section titled "Pathophysiology" be titled "Mechanism" instead per WP:MEDMOS? BakerStMD T|C 15:35, 15 January 2015 (UTC)

Either or is fine. We just recently added Mechanisms as an appropriate alternative. Doc James (talk · contribs · email) 23:26, 17 January 2015 (UTC)

Other Hypotheses

I just added a paragraph in the Other Hypotheses section describing Stanford Med's recent study which was published in Dec 2014. I worded it to reflect the findings of the study with mice, and quoted the lead investigator. The results of the test are published all over the internet. AtsmeConsult 15:35, 15 January 2015 (UTC)

I have removed it. For medical articles we typically stick with review articles. Press releases are not good sources. Neither are primary sources. That NSAIDS may affect AD development is already well discussed. Best Doc James (talk · contribs · email) 00:13, 16 January 2015 (UTC)
What about secondary and multiple reliable third party sources that wrote about it? I don't see why you removed the entire paragraph when you simply could have added an inline template for citation needed. Please talk to me in layman terms regarding NSAIDS and AD development. Where is it discussed? It obviously wasn't discussed in terms the average WP reader could understand. Thanks AtsmeConsult 02:41, 16 January 2015 (UTC)
For medical assertions, we have significantly higher standards on what constitutes a wp:RS. These are detailled at wp:MEDRS. This is a wp:FA seen by a huge number of readers, many of whom are affected directly by a disease that is generally recognized as one of the largest health challenges the world faces. We do not want to raise false hopes. Various discussions around one mouse study or another are classic examples of what we don't want. When there eventually is a substantial finding on the disease mechanism or a useful intervention, it will be backed up by independent corroboration and shouted from the rooftops. It will be reviewed in Nature, Lancet, or JAMA. We won't have to guess about whether it means something or whether to include it. Meanwhile there is wp:NODEADLINE. LeadSongDog come howl! 16:50, 16 January 2015 (UTC)
NSAIDS are discussed here Alzheimer's_disease#Medication Doc James (talk · contribs · email) 23:48, 17 January 2015 (UTC)

amyloid build up found in brains as young as 20 yo

Here's a couple of links to news articles re. finding amyloid build up in brains of people as young as 20 y.o. Could a regular editor add this info to the AD article?

Phantom in ca (talk) 22:49, 3 March 2015 (UTC)

We would need a medical review to add/cite this material; it's a bit premature anyway - the referenced primary source/study (apparently published March 2nd in a journal titled "Brain") isn't pubmed indexed as of writing this. Seppi333 (Insert  | Maintained) 00:44, 4 March 2015 (UTC)

Alois Alzheimer did not discover the disease Alois Alzheimer did not discover the disease nor did he claim to.--Wool Bridge (talk) 21:18, 4 March 2015 (UTC)

Ref says "In 1907, using the Bielschowsky stain on the case that made him famous, Alois Alzheimer described a startling new pathology in the brain of a recently deceased woman who died a few years after developing a clinically unusual dementia at age 51. The novel neuropathological feature that Alzheimer observed consisted of tangles of fibrils within the cyptoplasm of neurons, which were stained in sharp definition by the silver impregnation. His description included the following excerpt:" [6] Doc James (talk · contribs · email) 22:36, 4 March 2015 (UTC)
Was that wellcome trust piece published? Doc James (talk · contribs · email) 22:38, 4 March 2015 (UTC)


Results of a Phase II study of Aducanumab were released today.[7] I think they are notable and well-covered by multiple secondary sources. Thoughts? --Walter Siegmund (talk) 17:29, 20 March 2015 (UTC)

Is there a review on the topic? Doc James (talk · contribs · email) 23:37, 21 March 2015 (UTC)

"Study of thousands of brains reveals tau as driver of Alzheimer's disease", not amyloid

"By examining more than 3,600 postmortem brains, researchers at Mayo Clinic's campuses in Jacksonville, Florida, and Rochester, Minnesota, have found that the progression of dysfunctional tau protein drives the cognitive decline and memory loss seen in Alzheimer's disease. Amyloid, the other toxic protein that characterizes Alzheimer's, builds up as dementia progresses, but is not the primary culprit, they say.

The findings, published in Brain, offer new and valuable information in the long and ongoing debate about the relative contribution of amyloid and tau to the development and progression of cognitive dysfunction in Alzheimer's, says the study's lead author, Melissa Murray, Ph.D., a neuroscientist at Mayo Clinic in Jacksonville.

The findings also suggest that halting toxic tau should be a new focus for Alzheimer's treatment, the researchers say."


"Evidence suggests that abnormal tau then spreads from cell to cell, disseminating pathological tau in the brain's cortex. The cortex is the outer part of the brain that is involved in higher levels of thinking, planning, behavior and attention—mirroring later behavioral changes in Alzheimer's patients."

"Amyloid, on the other hand, starts accumulating in the outer parts of the cortex and then spreads down to the hippocampus and eventually to other areas," she says. "Our study shows that the accumulation of amyloid has a strong relationship with a decline in cognition. When you account for the severity of tau pathology, however, the relationship between amyloid and cognition disappears—which indicates tau is the driver of Alzheimer's," Dr. Murray says.


Please add to the main article as you think appropriate.

Phantom in ca (talk) 18:26, 24 March 2015 (UTC)

This debate has been going back and forth forever. We really need to wait until the findings are covered in reliable secondary sources before using them. An additional factor is that this new finding is not even being covered by the strongest popular science media, such as the New York Times, BBC, and Scientific American. It is only being covered by the plethora of science media that rely on press releases for their stories. When that happens, the chances are good that the story is not as significant as it may seem. Looie496 (talk) 20:09, 24 March 2015 (UTC)
Brain_(journal), where the research was published, is a professional, peer-reviewed journal published by Oxford U. Press. The research was not self-published. The research was, in fact, vetted by experts in the field prior to publication. NYT, BBC, SciAm: don't confuse popular media, even scientific popular media, with an Oxford U. professional peer-reviewed journal. They aren't even in the same league. BUT, for those who look to the MSM for scientifc/medical research, Bloomberg Business is now covering the story:
Do we have a high quality secondary source? Doc James (talk · contribs · email) 09:49, 27 March 2015 (UTC)
Phantom, the rules that govern our use of sources are embodied in WP:MEDRS. Regarding the underlying problem here, rather than writing a long explanation let me refer you to a blog post I wrote last year, The trouble with press release-based science reporting. The Bloomberg story is better than the others because it includes evaluations by independent experts -- but note that those experts are casting doubt on the significance of the study. Looie496 (talk) 14:32, 27 March 2015 (UTC)

New Section under Cause: Sleep Disruption

I am looking to make my first big edit to wikipedia. I would like to post a new section under causes entitled Sleep Disruption. Here is the bulk of that section. Please let me know if you have any suggestions before I attempt an edit to add this information.

A more recent explanation of Alzheimer's pathology postulates that sleep disruption can lead to or exacerbate already existing Alzheimer's Disease. Around 40% of Alzheimer's patients suffer from sleep disruption and it is the most common cause of institutionalization. [28][29] In general, sleep fragmentation has been found to correlate with the incidence of the disease and there are various explanations for this hypothesis.[30]

Slow wave sleep (SWS) is an important part of Non-rapid eye movement sleep that is implicated in facilitating memory consolidation. The amount of SWS is correlated with next day memory recall in healthy and Alzheimer's disease patients.[31] (add additional source) During SWS, mammals express two well defined oscillatory patterns, hippocampal ripples and cortical spindles. In Alzheimer's disease, patients show a decrease in time spent in SWS and a decreased ratio of SWS to REM sleep. Patients also show a reduction in fast spindles and overall spindle density, two measures which are associated with accuracy on memory recall tasks.[32] A reduction of SWS may lead to a breakdown of memory consolidation between the hippocampus and neocortex.[33]

Sleep disruption also adds a new dimension to the Amyloid hypothesis. In healthy patients, Aβ levels increase with wakefulness, but decrease during rest. In patients with Alzheimer's disease, there is less variability in Aβ, which remains high at night. This correlates with sleep disruption and increased wakefulness, which may lead to an overall increase in Aβ production.[34] Sleep disruption, therefore, could contribute to the build of Aβ proposed by the Amyloid hypothesis.

Another possible cause of sleep disruption is deregulation of hypocretin, melanin-concentrating hormone (MCH) and melatonin, three neuropeptides important in sleep and wakefulness. A deficiency in hypocretin is associated with sleeping disorders such as narcolepsy. Patients with Alzheimer's have decreased levels of hypocretin and hypocretin-1 neurons.[35] Low levels of hypocretin-1 has also been shown to correlate with increased sleep fragmentation in Alzheimer's.[36] If hypocretin levels are deregulated in Alzheimer's disease, then this could lead to poor sleep quality and therefore increased memory impairment.

MCH is correlated with Aβ levels and tau proteins associated with Alzheimer's. The levels of MCH in cerebral spinal fluid negatively correlate with memory. It has been suggested that misfolded tau protein tangles result in the hypersecretion of MCH, leading to daytime sleepiness and memory impairment.[37]

A potential treatment for Alzheimer's disease currently being tested is prolonged-release melatonin supplements. Melatonin improved sleep in Alzheimer's patients with and without insomnia, and it not only stopped memory decline, but improved performance after only 12 weeks. [38]KimonoKagaku (talk) 20:14, 11 April 2015 (UTC)

We need high quality secondary sources per WP:MEDRS. It is not clear your refs. Also please read WP:MEDMOS. We tend to avoid words like "suffer" and write in a more encyclopedic tone. Best Doc James (talk · contribs · email) 10:47, 12 April 2015 (UTC)
Agree with Doc ... please indicate your sources, and in addition to the pages above, review WP:RECENTISM and WP:NOT (news). Unless you have secondary reviews mentioning these items, it sounds speculative. SandyGeorgia (Talk) 19:44, 14 April 2015 (UTC)

Life expectancy and prognosis in the Introduction

"Although the speed of progression can vary, the average life expectancy following diagnosis is three to nine years.[4][5]"

This needs to be improved upon in a few ways. First, the citations aren't the best - one has a data spread from 1990 to 2011 I think (too wide surely for a general "is" statement like this) while the other is not readable at all for me - not even a couple of lines (a link issue?)

Background info: a number of people out there have survived this disease for 20 years now (since their first recorded signs - the person I care for has gone further and still lives at home with a full time carer and walks out daily, though language has almost gone down to a few single words like "thankyou" and the odd short habitual phrases interspersed with now-unrecognisable and mostly-meaningless gabble) -- and we know that the much shorter periods - like 2 or 3 years - can be linked to poor care. Certain care homes have little incentive to care beyond the time the average patient assets are depleted (ie around 3 years in the UK), while other establishments and many family carers go all out to make someone live as long as possible and can achieve stark differences. Care at its best is the most effective treatment of the disease, and has proved to be better that the drugs alone. In general, the better the general dementia care (which has improved over the years), the longer the patient lives. Care is of course linked to many things in dementia, which gradually increase as the suffer can does less - ranging from providing and monitoring diet to assuring continual hydration (which may not be mentioned enough in the article as it's the principle keyword in care) to simple attention, exercise, suitable activity and stimulus. I realise that all this has to be cited if included in the main page, but it still needs to be taken into consideration when structuring the other lines.

Also this detail on prognosis needs to be better/clearer on 'onset time' (which is hard to know of course) and 'diagnosis time' - which could be as any point down the line. Diagnosis of course gets better all the time. Currently we have very selective and out of date averages leading to a classic Wikipedia definitive (ie an x "is" y line).

If ever there was a detail to keep an eye on and attempt to improve upon, it is this one. It's barely changed in 10 years. I think in 2006 I edited this article a number of times, and wasn't that happy with whatever the figure was then. Remember that some people in referenceland have something akin to a vested interest in keeping the longevity figures down too: so the 3 year figure still gets touted a lot - far too much in my opinion as it represents a negative outlook. The person I mentioned about was given 6 months to get to the stage I described - now over 10 years ago. She was going down hill fast at the time, but her condition was actually reversed a degree and then drastically slowed. In the UK we are having a torrid time with various scandals on this issue - that of poor care basically. It skewers figures terribly. There is no money to be made in general public care. It's just an unfortuate reality I'm afraid - it all needs government subsidy really. The funding is never enough for the fully required level of care in all but the most select of care homes. With Alzheimer's you go down like a lead balloon without a sufficient level of care - it's terrifying to see how quickly people can drop (or be lifted a bit too if you are lucky - it can be very hard to see what's gone without taking the effort to look). Everytime I see a new and "existing" set of potential-treatment results ("ready within 10 years!"), it always strikes me how different the approach is to the last one I read. They just don't know enough about this disease I'm afraid.

Anyway, a couple of tight lines need to be written that cover the past and the potentials re prognosis. I've had time to write this, but I'd appreciate it if someone else had a good look at it. Matt Lewis (talk) 03:32, 6 May 2015 (UTC)


Two papers in JAMA about the role of amyloid (doi:10.1001/jama.2015.4668 and doi:10.1001/jama.2015.4669). May be worth discussing. JFW | T@lk 14:50, 20 May 2015 (UTC)

I wonder if the connection made to age in the articles correlate with, plausibly, an individuals decline in diet? Do elderly individuals have a higher likeliness to deposit heavy metals? DeadFire999 (talk) 19:51, 20 May 2015 (UTC)

Alzheimer's disease - cause may be connected to 6 genes involved in brain development

Is this study worth mentioning in the article? The study finds evidence that 50,000 to 200,000 years ago, natural selection drove changes in six genes involved in brain development. These changes may have helped to increase the connectivity of neurons, making modern humans more intelligent, but an effect was the same genes are implicated in Alzheimer's disease. Jcardazzi (talk) 12:25, 27 May 2015 (UTC)jcardazzi

We discuss the generics here Alzheimer's_disease#Genetics. Best to use review articles though. Doc James (talk · contribs · email) 03:07, 28 May 2015 (UTC)
Like Doc James stated, the easiest way to keep an edit from being reverted by another user or bot is to reference studies that are; 1) In my personal opinion, not epidemiological. 2) Peer reviewed, or reviewable. 3) Or a socially accepted, and accreditable, sources! (e.g. PubMed) DeadFire999 (talk) 06:05, 2 June 2015 (UTC)

Misinformation, Presenting New Study

Under Other hypotheses it is stated "other studies have concluded that there is no relationship between these environmental factors and the development of AD." and links to a 2002 article that claims "not enough epidemiological evidence supports a link between aluminum in drinking water and AD"[1]. As there may not be not have been enough evidence in 2002 to link the alum in drinking water, I present a new study claiming a link between the brain translocation of alum particles to a Trojan horse mechanism, that is seen in infectious particles like HIV, that obeys to CCL2, signaling the major inflammatory monocyte chemoattractant.[2] DeadFire999 (talk) 05:25, 12 May 2015 (UTC)

The paper you link does not mention AD? Some reviews do support a possible link. [8] Doc James (talk · contribs · email) 05:36, 12 May 2015 (UTC)

No, it does not directly claim a link to AD, but does claim a link to the CCL2 cytokine which is linked to AD. [3]DeadFire999 (talk) 05:59, 12 May 2015 (UTC)

I would also like to link the following reference. [4] DeadFire999 (talk) 10:27, 12 May 2015 (UTC)

Yes very tentative. A discussion in the research section is needed. Doc James (talk · contribs · email) 18:06, 12 May 2015 (UTC)
Doctor, I would also like to present another study for your review. My apologies if you have already seen it. [5] DeadFire999 (talk) 21:43, 12 May 2015 (UTC)
  • Some of these are a little old. Others are primary sources
  • Frontiers in Neurology also has a low impact factor of 0.936
  • This review is interesting [9]

Doc James (talk · contribs · email) 22:47, 12 May 2015 (UTC)

I'm not certain how much of what PMID 24806729 says can be regarded as truly secondary. "We previously showed" flags the fact that the reviewers are citing their own prior works. It would need great care if used. The rest clearly don't meet wp:MEDRS, they are either too old, primary, or in one case wp:CIRCULAR. They might be useful for off-wiki work, but we couldn't use them. Please don't be discouraged though, and by all means do continue discussing possibilities. LeadSongDog come howl! 13:24, 2 June 2015 (UTC)
Could you elaborate more LeadSongDog, I'm not sure which of the articles I shown you have a contradiction with. I do believe that the majority are from 2014 and 15. Yes, I did in one case do a circular reference, but that was to save time and space to link to references already added on another link. Thank you for your time. DeadFire999 (talk) 13:40, 2 June 2015 (UTC)
  • Sure. You listed:
  • PMID 12222737 which is long out of date
  • PMID 25699008 which is not really secondary, the authors are reviewing their own prior papers
  • CCL2#Clinical importance which is circular (and the ref list there is horribly bad itself)
  • PMID 25206046 which is clearly primary
  • PMC 4155793 which is an opinion paper, again the authors are citing themselves

Thank you LeadSongDog for your reply, although I do have a few objections. I wouldn't mind discussing this further if you so choose.
  • I referenced to PMID 12222737 (As does the main article) to contest the use, not condone.
  • PMID 25699008 references a total of 95 different works, although a few of the articles referenced some of the authors had participated in. G. Crepeaux did not co-author any of the linked references in that article, nor did H. Eidi. As for the few articles that have similar authors Gherardi and Authier, appear the most and usually together with other researchers. Cadusseau appears in one referenced source. So I do not feel they are simply reviewing their own papers, more so they are used in support of other references made.
  • I knew the CCL2 link was circular, but I assumed that is was generally accepted that CCL2 signaled inflammation and did not feel a necessity to reference outside sources on the talk page.
  • PMID 25206046 is a very well conducted study. Although it is suggested to rely on secondary sources, it is not a requirement listed in MEDRS. As for the 'ban' on primary papers, it seems very diluting to the dissemination of information. My reason is that although some studies are not done properly, the ones that are face being forgotten and never reviewed making them useless to us at Wiki. I believe due diligence is necessary before posting primary though. Further more, say if a secondary source agreed with a primary source which was flawed, wouldn't that make that secondary review equally as flawed and therefor unreliable?
  • Also in PMC 4155793 I do not see only referenced works of the authors. I was told a prase once that goes; "If you're right, then you are right." For that reason I see no harm in collating papers into a review to correlate facts. Even if you happened to help in a few!
  • Mainly I wanted to bring the study to light in hopes that someone, who is capable to perform a secondary study, will take interest and review there findings. I, personally, feel that an in-depth study into adjuvents is essential to avoid a public health crisis. Or at least mitigate the harms already caused. Primum non nocere! DeadFire999 (talk) 08:13, 3 June 2015 (UTC)
To contest the use, it is simpler to flag the use with {{medrs}}, which will draw editors' attention to the trouble spot. If a more current secondary source is identified supporting the same statement, it is helpful to accompany that with hidden text suggesting the new alternative. If the statement is invalidated by the current science it should either be wp:BOLDly fixed or flagged for attention. The {{dubious}} template is good for this purpose.
Review authors looking at primary work are often more inclined to assume their own papers were correct. That is why we seek independent reviewers. Regarding PMID 25699008, Gherardi authored refs 3,4,21,45,46,49,84,89. Authier 3,5,10,19,21,40,43,45,46,49,78. Cadusseau 45. Eidi and Crépeaux authored none of them. If the WP assertion is based on work other than those parts, fine. But if our assertion is based on any of those 14 primary source papers, (especially source 45) then we can't trust it.
We don't treat links to wikipedia articles as references, we would simply wikilink CCL2 when mentioning it. However, any statement about it in the context of AD would still need citation to a valid source that supports the statement.
"PMID 25206046 is a very well conducted study" is an example of wp:OR. I think your statement is quite probably correct, but how are readers to know that? Your (and my) opinion of the study are irrelevant here because we are pseudonymous, and readers have no way to assess our credibility. Accordingly, we mustn't make our own assertions.
"If you're right you're right" and you should publish. Just not on Wikipedia. When someone independent agrees in a reliably published review, we'll pick it up. Wikipedia has wp:NODEADLINE, so we can wait a few months. We don't need to be breaking news. A conclusive result on the etiology of AD will probably win a Nobel. It will certainly make the cover of a major journal (Nature, JAMA, etc.) Rest assured that it won't be buried in Frontiers in Neurology. That journal uses a tiering system described here that is vulnerable to being gamed by creating "buzz" in social media. We won't be enablers for such gaming.
Many people are desperate for answers that just don't exist yet, so "non nocere" includes not raising false hopes. We've been around the loop on this many times with various candidate therapies that didn't pan out.
Don't take this wrong, but I get the sense that your wiki-skills might be better developed by working first on some lower profile articles. This one is a top-importance featured article, and it gets a lot of attention. We have to be particularly careful with it. Perhaps you could start with improving that CCL2 article? It certainly could use it. LeadSongDog come howl! 18:39, 3 June 2015 (UTC)
Thank you LeadSongDog, I very much appreciate your assistance. DeadFire999 (talk) 05:41, 4 June 2015 (UTC)


rewriting a sentence

I would like to change this sentence in the third paragraph: "There are no medications or supplements with evidence to support their use" to this: "There are no medications or supplements that have been proven by scientific study to treat Alzheimer's."

Does anyone mind? Rissa, Guild of Copy Editors (talk) 03:24, 19 June 2015 (UTC)

Have clarified it to "There are no medications or supplements that decrease risk." This was refering to prevention rather than treatment. Doc James (talk · contribs · email) 07:29, 19 June 2015 (UTC)

coconut oil/MCTs and AD: providing an alternative fuel for the AD afflicted brain

I came across this video a few years ago:

Later, I saw this video where the head of USF's Byrd Alzheimer's Institute says they're undertaking a human trial to study its effectiveness:

I saw on the Byrd's website that the study is still in progress.

However, when I went to the Wiki page on MTCs I found this citation that supports the theory behind their use. Stafstrom CE, Rho JM (2012). "The ketogenic diet as a treatment paradigm for diverse neurological disorders". FRONTIERS IN PHARMACOLOGY. 3: Article 59. PMC 3321471Freely accessible. PMID 22509165. doi:10.3389/fphar.2012.00059. 

I also found this study (2015) which also supports the theory that AD involves impaired glu uptake by affected neurons and that ketone bodies can provide an alternative energy source.Castellano; et al. (2015). "Lower Brain 18F-Fluorodeoxyglucose Uptake But Normal 11C-Acetoacetate Metabolism in Mild Alzheimer's Disease Dementia". Journal of Alzheimer's Disease. 43. doi:10.3233/JAD-141074.  Unknown parameter |no= ignored (help) From the abstract: Background: The cerebral metabolic rate of glucose (CMRg) is lower in specific brain regions in Alzheimer's disease (AD). The ketones, acetoacetate and β-hydroxybutyrate, are the brain's main alternative energy substrates to glucose..... Conclusion: Regional brain energy substrate hypometabolism in mild AD dementia may be specific to impaired glucose uptake and/or utilization. This suggests a potential avenue for compensating brain energy deficit in AD dementia with ketones.

I think MCTs (and coconut oil as a source), should be mentioned in the main page's dietary section as a possible treatment, esp. since there is little downside to its use. Phantom in ca (talk) 23:38, 13 June 2015 (UTC)

Please see WP:MEDRS. Doc James (talk · contribs · email) 14:49, 22 June 2015 (UTC)

AD as Type III diabetes: another entry for "Causes: Other Hypothesis"?

Here is a secondary source study reviewing the hypothesis that AD is a type of diabetes mellitus of the brain (Type III Diabetes).

"Alzheimer's Disease Is Type 3 Diabetes–Evidence Reviewed" J Diabetes Sci Technol. 2008 Nov; 2(6): 1101–1113. PMCID: PMC2769828 The study is online at:

Please add it to the main article if suitable. Phantom in ca (talk) 18:40, 25 June 2015 (UTC)

Journal has no impact factor per [10]. Therefore it is not suitable. This hypothesis has been bandied around for years. It has gained significant traction though. Doc James (talk · contribs · email) 18:53, 25 June 2015 (UTC)

Omentum transposition (OT) onto the AD brain surgery

This is something else I want the Wiki AD "community" to know about. Looks like it is still experimental (after ~20 years), but at least it is not totally off the radar screen. It is a treatment, not a cure. IMO, it may be a "bridge" to allow some to maintain cognitive function while awaiting other treatments or a cure.

This appears to be the first article by Dr. Goldsmith re OT & AD, although he did OT for decades prior for other, incl CNS, ailments.


appears to be a reprint (w/o images) of this study:

Looks like other researchers have had positive results in treatment of AD w/OT too:

Looks like a new study is getting underway right now:

Here's a text Dr. Goldsmith edited re the omentum:

Last, here's another article by Dr. Goldsmith:

Sure it is way premature to add this to the main article. But I wanted to get this info posted for Wiki AD folks to monitor in case I'm not able to....

Phantom in ca (talk) 20:13, 26 June 2015 (UTC)

Thanks. Appears to be all one person. Doc James (talk · contribs · email) 20:25, 26 June 2015 (UTC)

Phantom in ca here again. Not sure if I'm editing/posting this right. Doc James, I've bolded "other researchers" and "new study" above. Neither of those studies, as far as I can tell, involve Dr. Goldsmith. Phantom in ca (talk) 02:01, 27 June 2015 (UTC)

Interesting. Hopefully we will get a high quality review of the topic soon. Doc James (talk · contribs · email) 02:32, 27 June 2015 (UTC)

Amyloid hypothesis − a review in Nature Neuroscience

David Holtzman has published a review in Nature Neuroscience on the amyloid hypothesis as the mainstream one for research in AD ( It seems like it could be a good source to brush up the section on causes, that looks a bit outdated. Fedor Babkin (talk) 12:35, 2 July 2015 (UTC)

The abstract certainly looks promising. From what little I can see, they advance the Aβ-as-trigger-of-tau-aggregation argument. Are Nature "perspective" articles usually treated as secondary, or is the reasoning advanced by the authors considered as primary?
Fuller citation:
The article is paywalled until 26 May 2016.

LeadSongDog come howl! 15:23, 2 July 2015 (UTC)

I have the full text. It is a review, it doesn't include any ideas that might be regarded as primary. --Fedor Babkin (talk) 17:51, 5 July 2015 (UTC)

article about early detection and potentially halting progress of alzheimers

this article looks to be very interesting - I'm guessing there are things that could be added/updated based on it? EdwardLane (talk) 06:06, 18 July 2015 (UTC)

It's early days yet, Edward. Once the research has advanced a bit and it's been reviewed by independent experts in academic journals, then there may be a place for it in this article. Maybe in early development, should it reach that stage, it could have a section in Alzheimer's disease research. But it's too early for us to report now. --Anthonyhcole (talk · contribs · email) 00:04, 31 July 2015 (UTC)

Stages of Alzheimer's disease info box

There appears to be an error in this info box. The two points "Minor short-term memory loss[18]; Forgetting that memory lapses happened[18]" seem to have been swapped with these two points "Absent-mindedness[18]; Forgetting appointments[18]". The current (5/07/2015) writing contradicts that of the paper that the info box references. Can someone with the correct permissions correct this error.

On closer inspection, the two points "Speech impairment[18]; Repeatedly initiating the same conversation[18]" have also been swapped with "More aggressive or passive[18]; Some loss of self-awareness[18]". This is a total of 8 errors, and means the half the info box contradicts its reference. Can someone immediately correct this error. — Preceding unsigned comment added by Willb32764 (talkcontribs) 22:52, 4 July 2015 (UTC)

User:Willb32764 we cannot do to copyright law use their wording verbatim. We must paraphrase.
"More aggressive or passive" is a reasonable summary of "Neglect of personal hygiene. Personality changes; may become abusive" Doc James (talk · contribs · email) 00:14, 5 July 2015 (UTC)

My issue is not with the paraphrasing, it is with the paraphrased statement being placed under the wrong heading. On page 5, Table 1, "May become more aggressive or passive" is under the Middle-Stage. I am ok with paraphrasing this to "More aggressive or passive", however it has been placed under the Late-Stage heading for some reason. The other 7 paraphrased statements have also being placed under the wrong heading. Can this be corrected? — Preceding unsigned comment added by Willb32764 (talkcontribs) 01:24, 5 July 2015 (UTC)

I've removed it for now and will look into it in about 12 hours. --Anthonyhcole (talk · contribs · email) 00:54, 31 July 2015 (UTC)
Fixed it Doc James (talk · contribs · email) 09:53, 31 July 2015 (UTC)
Thank you, James. --Anthonyhcole (talk · contribs · email) 10:18, 31 July 2015 (UTC)

Citations: time to revisit vcite vs cite ?

A discussion at User_talk:Magioladitis#Alzheimer.27s_disease has once again brought up the question. Some years ago, when {{cite journal}} was very slow, this article was a poster child for slow loading html. In response, we expediently changed them to {{vcite journal}}. That solved the performance issue, but stripped out some of the metadata and linking functionality. Since then, the template code switch to Lua has addressed the performance issue generically. Further, over recent months instances of the {{cite journal}} template have crept back in. This is complicated by adding vcite2 to the mix. As wp:WIAFA calls for consistent citation style, I would suggest that it may be time to make them all the same, and further recommend a return to cite journal but using the new |vauthors= as the cleanest functional choice. Clearly this will require consensus to implement. The default alternative would be to standardize on the predominant existing style. Are there any serious concerns, or just personal preferences at issue? LeadSongDog come howl! 17:55, 5 August 2015 (UTC)