Talk:Alpha-synuclein

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Untitled[edit]

I would like to ask about "In melanocytic cells, SNCA protein expression may be regulated by MITF.[5]". I have checked a cited paper but I could not find anything about alpha-synuclein. Where does it come from? —Preceding unsigned comment added by 158.93.6.11 (talk) 22:27, 2 February 2010 (UTC)[reply]

Checking supplementary material in the paper, alpha synuclein comes out in the tables. However there could be some reasonable WP:OR concern in how the thing is phrased. Thank you for coming to the talk page, and consider making an account if you want to discuss/edit further, given that your IP is shared. --Cyclopia ^talk 22:35, 2 February 2010 (UTC)[reply]

Parkinson's is not an amyloid disease[edit]

"alpha-synuclein can aggregate to form insoluble amyloid fibrils in pathological conditions". According to the litterature, Parkinson's does not fall under the category "Amyloidosis" as it does not involve amyloids. See e.g. Pepys MB (2006) Amyloidosis. Annu. Rev. Med., 57: 223-241. I have removed the word "amyloid". Silasmellor (talk) 18:53, 20 April 2010 (UTC)[reply]

Pepys' main point is "In genuine amyloidosis, the deposits are unequivocally harmful, and measures to prevent their formation and/or promote their removal are clinically beneficial."

In other words he defines amyloidosis as meaning that the amyloid deposits are known to be causal of the disorder. They are *still* amyloid deposits by any reasonable definition of the word. By Silasmellor's definition, the deposits in Alzheimer's disease are also not amyloid. (Pepys includes AD as a non-amyloidosis in the 2006 ARM article.) The peptide present in the plaques is called "amyloid-beta peptide." To be accurate here we should be clear that PD and AD are suspect amyloidoses because the proteins associated with them are observed to form amyloid plaques as one of the symptoms. Therefore it is entirely appropriate to use the term amyloid. 70.42.157.5 (talk) 19:05, 6 February 2014 (UTC)[reply]

Agreed. Amyloid is the appropriate word. PD and AD are suspected amyloidosis as the causative role of the amyloid in both pathologies has not been fully established. 157.139.173.156 (talk) 15:12, 15 May 2018 (UTC)[reply]

Cloaking process as enabler of correct folding[edit]

Why has no more recent research been included for 12 years and the asynuclein research at a standstill? Eclessia (talk) 04:13, 10 October 2016 (UTC)[reply]

Structure[edit]

The structure section is wholly inappropriate. There are not appropriate citations and the short paragraph does not properly discuss the various known structural forms of α-synuclein. 157.139.173.156 (talk) 15:13, 15 May 2018 (UTC)[reply]

SNCA vs Alpha-synuclein[edit]

It seems to me that there are two topics on this page - the SNCA gene, and alpha-synuclein. Should they be separate pages?

On the right, the first picture is of a molecule of alpha-synuclein, but the heading is 'SNCA', and the detail in the panel below this is all about the SNCA gene. Whereas the body of the page, and the illustrations further down, are all to do with alpha-synuclein, apart from a brief mention of the gene in the leading paragraphs (twice, the same phrase being repeated).

Do you see my puzzlement?

Issues related to MOS:LEAD[edit]

The main problem, as I see it, is that a lot is mentioned in the lead that's not in the body of the article. MOS:LEAD says The lead serves as an introduction to the article and a summary of its most important contents. and a lead section should .... be carefully sourced as appropriate. For example, there's nothing about NACP except in the lead (and some references within the body but the term is not used there). The lead seems to have way too many references, most (14) of which are not used elsewhere, which is odd if it is a summary. My conclusion is that the body of the article needs expansion and then the lead can be re-written as per MOS:LEAD.

Following an exchange at the Teahouse, I think that the main reason for the term "NACP" not being used in the body of the article is owing to the history of the subject. There are sentences at the end of the lead It was later determined that NACP was the human homologue of Torpedo synuclein. Therefore, NACP is now referred to as human alpha-synuclein. A reference for this^[1] should be included and the same sort of comment made in the body (or maybe only there). Further references related to the discovery of alpha-synuclein in filaments in Parkinson’s disease, Lewy bodies and multiple system atrophy are available.^[2]^[3]

References

^ Jakes, Ross; Spillantini, Maria Grazia; Goedert, Michel (1994). "Identification of two distinct synucleins from human brain". FEBS Letters. 345 (1): 27–32. doi:10.1016/0014-5793(94)00395-5. PMID 8194594. S2CID 36840279.
^ Spillantini, M. G.; Crowther, R. A.; Jakes, R.; Hasegawa, M.; Goedert, M. (1998). "α-Synuclein in filamentous inclusions of Lewy bodies from Parkinson's disease and dementia with Lewy bodies". Proceedings of the National Academy of Sciences. 95 (11): 6469–6473. doi:10.1073/pnas.95.11.6469. PMC 27806. PMID 9600990.
^ Spillantini, Maria Grazia; Crowther, R. Anthony; Jakes, Ross; Cairns, Nigel J.; Lantos, Peter L.; Goedert, Michel (1998). "Filamentous α-synuclein inclusions link multiple system atrophy with Parkinson's disease and dementia with Lewy bodies". Neuroscience Letters. 251 (3): 205–208. doi:10.1016/S0304-3940(98)00504-7. PMID 9726379. S2CID 54366155.

I'm not confident about making a good job of re-writing anything as it is beyond my speciality but I hope my comments will encourage others — Boghog perhaps — to do so. Mike Turnbull (talk) 14:50, 7 April 2021 (UTC)[reply]

@Michael D. Turnbull and 11mgs: Just trying to figure out what exactly is the issue here since I see no recent edits to this article by 11mgs. I do see that the second paragraph of the lead has issues and probably should be moved to the function section. The third paragraph of the lead is at least mentioned in the clinical significance section, but should be rebalanced. Do my proposed edits address the concerns? Context: Teahouse: editing of wikipedia pages. Cheers Boghog (talk) 15:55, 7 April 2021 (UTC)[reply]

That's correct, Boghog, there were no edits here, only suggestions regarding the references that could be included, as above. Thanks for re-doing the lead and moving some other material to the body. All is now much better in my opinion. I've added Ref 1 from this discussion to the point in the lead where 11mgs suggested it should go to back up the statement about the "later" paper. I'll leave any further discussion / additions to you both. Mike Turnbull (talk) 07:22, 8 April 2021 (UTC)[reply]

Clarrification on Mitochondrial Role[edit]

Under the "Tissue Expression" heading, it is stated that " Alpha-synuclein is highly expressed in the mitochondria in olfactory bulb, hippocampus, striatum and thalamus...". This is at best confusing.

Initially, I took it to mean that alpha-synuclein is encoded in mitochondrial DNA, but other parts of the article make it clear that (in humans) the gene is on chromosome 4. If so, what does the "highly expressed in" phrasing mean? I don't know enough to be sure (hence I won't edit it), but I'm guessing that the intended meaning is something like "Alpha-synuclein is highly expressed from nuclear DNA in the olfactory bulb, hippocampus, striatum and thalamus, whence it is transported to, and occurs mainly in, the mitochondria". Probably this is how experts will read it anyway, but for generalists it is not the natural reading. For example, I am still wondering whether it is possible that the mRNA is transcribed off the nuclear DNA, but then transported into mitochondria and translated by the mitochondrial ribosome, thus justifying the "expressed in" phrasing (though the differences in nuclear and mitochondrial coding make that seem unlikely).

Please, if you know what the intended meaning is here, could you edit to clarify it. Urilarim (talk) 00:55, 13 April 2023 (UTC)[reply]

[pmid8194594-1] Jakes, Ross; Spillantini, Maria Grazia; Goedert, Michel (1994). "Identification of two distinct synucleins from human brain". FEBS Letters. 345 (1): 27–32. doi:10.1016/0014-5793(94)00395-5. PMID 8194594. S2CID 36840279.

[pmid9600990-2] Spillantini, M. G.; Crowther, R. A.; Jakes, R.; Hasegawa, M.; Goedert, M. (1998). "α-Synuclein in filamentous inclusions of Lewy bodies from Parkinson's disease and dementia with Lewy bodies". Proceedings of the National Academy of Sciences. 95 (11): 6469–6473. doi:10.1073/pnas.95.11.6469. PMC 27806. PMID 9600990.

[pmid9726379-3] Spillantini, Maria Grazia; Crowther, R. Anthony; Jakes, Ross; Cairns, Nigel J.; Lantos, Peter L.; Goedert, Michel (1998). "Filamentous α-synuclein inclusions link multiple system atrophy with Parkinson's disease and dementia with Lewy bodies". Neuroscience Letters. 251 (3): 205–208. doi:10.1016/S0304-3940(98)00504-7. PMID 9726379. S2CID 54366155.

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