Prevention of dementia

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Prevention of dementia is the attempt to avoid developing dementia. Although no cure for dementia is available, there are many ways to decrease the risk of acquiring dementia in the first place, including both lifestyle changes and medication.

Lifestyle[edit]

Mental activity[edit]

Main article: Brain fitness

"Use it or lose it" might be applied to the brain when it comes to dementia. Intellectual activities help keep the mind in shape in later years. Activities such as reading, playing cards and board games and playing a musical instrument can postpone the onset and slow the progression of both Alzheimer's and vascular dementia.[1] The risk decrease is proportional to frequency of activity,[1] with slower cognitive decline being associated with both late-life and early-life increased cognitive activity.[2]

Aside from spare time activities, a mentally demanding occupation may prevent dementia, especially during the thirties, forties and fifties.[1]

Mental activity may help to prevent dementia by building up a "brain reserve": additional connections between neurons are created which are more resistant to the deterioration seen in dementia.[1]

Physical activity[edit]

Since vascular dementia is the second most common form of dementia (after Alzheimer's disease), reducing the risk of cerebrovascular disease also reduces the risk of dementia. Thus, physical exercise, having good blood cholesterol, healthy body weight and blood pressure lowers the risk of developing dementia.[1] An active lifestyle can almost halve the risk compared to a sedentary one.[1]

The effect of physical activity is not limited to vascular effects. For instance, it can give rise to new neurons in the brain, as well as releasing a substance that can protect them.[1] The protein known as Brain Derived Neurotropic Factor (BDNF) is known to be important in the development, survival and plasticity of Neurons, regular exercise can boost BDNF levels by 2-3 times.[3]

Some studies say Alzheimer's and other dementias may be caused by high blood pressure, since it can cause blood vessel damage through constriction.[4][5]

Diet[edit]

Obesity increases the risk of any dementia and Alzheimer's disease in particular.[1] The effect of alcohol on the risk of dementia is a J curve:[6] high alcohol consumption increases the risk of dementia[7] while low alcohol consumption may be protective.[6] However, low alcohol consumption may not protect against vascular dementia and overall cognitive decline.[6] Moderate alcohol consumption can possibly reduce the risk of vascular disease and dementia because it can increase blood levels of HDL cholesterol and weakens blood-clotting agents such as fibrinogen, which offers some protection against heart attacks and small subclinical strokes that together can ultimately damage the brain.[8] The effects of omega-3 fatty acid in the prevention of dementia is uncertain.[9] Vegetables and nuts may be of benefit,[1] because of their high content of polyunsaturated fats. Non-fish meat, on the other hand, increases the risk of Alzheimer's,[1] because of its high content of saturated fat. However, consumption of fish should be limited due to concerns over mercury poisoning, which could exacerbate the symptoms of dementia. Estrogen may also help in the prevention of dementia but cannot help when dementia is already present and when cognitive function is already impaired. It increases cerebral blood flow and is an anti-inflammatory agent, enhancing activity at the neuronal synapses in the brain. It may also help to increase brain activation in regions that are affected by dementia which is mainly the hippocampus region.[10] Niacin (vitamin B3) is also believed to prevent dementia as research shows those who have the highest levels of niacin in their blood, are believed to have the lowest risk of developing dementia or having cognitive decline. Niacin is involved with DNA synthesis and repair and also neural cell signaling, it improves circulation and reduces cholesterol levels. In order for niacin to have a positive effect on the brain, it is recommended that patients have 100 to 300 mg per day.[8]

Sleep pattern[edit]

More than nine hours of sleep per day (including daytime napping) may be associated with an increased risk of dementia.[11]

Medication[edit]

Hypertension medications[edit]

The etiology of vascular dementia includes hypertension, and thus, lowering blood pressure with antihypertensives may have a positive effect in the prevention of dementia, just as physical activity.

However, a study failed to demonstrate a link between high blood pressure and developing dementia. The study, published in the Lancet Neurology journal July 2008, found that blood pressure lowering medication did not reduce the incidence of dementia to a statistically significant degree. A prospective meta-analysis of the data from this study with other studies suggested that further research might be warranted.[12]

Anti-diabetic drugs[edit]

Diabetes mellitus is a risk factor for vascular dementia, and is thus the risk is lowered with anti-diabetic drugs.[13]

Besides, Rosiglitazone (Avandia) improves memory and thinking ability for people with mild Alzheimer's disease. The mechanism of the effect may be the ability of the drug to reduce insulin resistance.[1] Thus, less insulin needs to be released to achieve its metabolic effects. Insulin in the bloodstream is a trigger of amyloid beta-production,[13] so decreased insulin levels decrease the level of amyloid beta. This leads to less formation of amyloid plaques seen in Alzheimer's disease.

NSAIDs[edit]

Non-steroidal anti-inflammatory drugs (NSAIDs) can decrease the risk of developing Alzheimer's and Parkinson's diseases.[1] The length of time needed to prevent dementia varies, but in most studies it is usually between 2 and 10 years.[14][15][16][17][18] Research has also shown that it must be used in clinically relevant dosages and that so called "baby aspirin" doses are ineffective at preventing and treating dementia.[19]

Alzheimer's disease causes inflammation in the neurons by its deposits of amyloid beta peptides and neurofibrillary tangles. These deposits irritate the body by causing a release of e.g. cytokines and acute phase proteins, leading to inflammation. When these substances accumulate over years they contribute to the effects of Alzheimer's.[20] NSAIDs inhibit the formation of such inflammatory substances, and prevent the deteriorating effects.[21][22][23]

Vaccine[edit]

There is as yet no vaccine against dementia.[1] Such a vaccine could activate the body's own immune system to combat the beta amyloid plaques in Alzheimer's disease. One problem to overcome is overreaction from the immune system, leading to encephalitis.[1]

See also[edit]

References[edit]

  1. ^ a b c d e f g h i j k l m n Thoenen, Eugenia; Health Statistics Center Statistical Staff; Doria, James; King, Fred; Leonard, Thomas N.; Light, Tom; Simmons, Philip (February 2005). "Prevention of Dementia". Dementia: The Growing Crisis in West Virginia. Retrieved 2 October 2009. 
  2. ^ Wilson, Robert S., et al. (July 3, 2013). "Life-span cognitive activity, neuropathologic burden, and cognitive aging (Abstract)". Neurology. Archived from the original on July 5, 2013.  Explained by Koren, Marina (July 23, 2013). "Being a Lifelong Bookworm May Keep You Sharp in Old Age". Smithsonian. Archived from the original on July 5, 2013. 
  3. ^ Jones, Hilary. "Dr". http://www.telecare24.co.uk/blog/dr-hilary-jones-preventing-dementia-exercise/. 
  4. ^ "Blood pressure drug dementia hope". BBC News. 28 July 2008. Retrieved 2 October 2009. 
  5. ^ "Blood Pressure Drugs May Protect Against Alzheimer's" (Press release). Boston University School of Medicine. 27 July 2008. Retrieved 2 October 2009. 
  6. ^ a b c Chen JH, Lin KP, Chen YC (October 2009). "Risk factors for dementia". J. Formos. Med. Assoc. 108 (10): 754–64. doi:10.1016/S0929-6646(09)60402-2. PMID 19864195. 
  7. ^ Grønbaek M (April 2009). "The positive and negative health effects of alcohol- and the public health implications". Journal of Internal Medicine 265 (4): 407–20. doi:10.1111/j.1365-2796.2009.02082.x. PMID 19298457. 
  8. ^ a b Robert, Levine (2006). "Defying dementia: understanding and preventing Alzheimer's and related disorders". Westport: conn: Praeger. 
  9. ^ Cederholm T, Palmblad J (March 2010). "Are omega-3 fatty acids options for prevention and treatment of cognitive decline and dementia?". Current Opinion in Clinical Nutrition and Metabolic Care 13 (2): 150–5. doi:10.1097/MCO.0b013e328335c40b. PMID 20019606. 
  10. ^ Eileen M., Welsh (2003). "Focus on Alzheimer's disease research". Nova Biomedical books: 699. 
  11. ^ Benito-León, J; Bermejo-Pareja, F; Vega, S; Louis, ED (2009). "Total daily sleep duration and the risk of dementia: a prospective population-based study". European journal of neurology 16 (9): 990–7. doi:10.1111/j.1468-1331.2009.02618.x. PMID 19473367. 
  12. ^ Peters R1, Beckett N, Forette F, Tuomilehto J, Clarke R, Ritchie C, Waldman A, Walton I, Poulter R, Ma S, Comsa M, Burch L, Fletcher A, Bulpitt C; HYVET investigators (August 2008). "Incident dementia and blood pressure lowering in the Hypertension in the Very Elderly Trial cognitive function assessment (HYVET-COG): a double-blind, placebo controlled trial". Lancet Neurol 7 (8): 683–9. doi:10.1016/S1474-4422(08)70143-1. PMID 18614402. Retrieved 10 April 2014. 
  13. ^ a b "Diabetes and Alzheimer's linked" (Press release). Mayo Clinic. 6 November 2008. Retrieved 2 October 2009. 
  14. ^ Szekely, CA; Green, RC; Breitner, JC; Østbye, T; Beiser, AS; Corrada, MM; Dodge, HH; Ganguli, M; Kawas, CH (2008). "No advantage of "Aβ42-lowering" NSAIDs for prevention of AD in six pooled cohort studies". Neurology 70 (24): 2291–8. doi:10.1212/01.wnl.0000313933.17796.f6. PMC 2755238. PMID 18509093. 
  15. ^ Cornelius, C; Fastbom, J; Winblad, B; Viitanen, M (2004). "Aspirin, NSAIDs, risk of dementia, and influence of the apolipoprotein E epsilon 4 allele in an elderly population". Neuroepidemiology 23 (3): 135–43. doi:10.1159/000075957. PMID 15084783. 
  16. ^ Etminan, M; Gill, S; Samii, A (2003). "Effect of non-steroidal anti-inflammatory drugs on risk of Alzheimer's disease: systematic review and meta-analysis of observational studies". BMJ 327 (7407): 128. doi:10.1136/bmj.327.7407.128. PMC 165707. PMID 12869452. 
  17. ^ Nilsson, SE; Johansson, B; Takkinen, S; Berg, S; Zarit, S; Mcclearn, G; Melander, A (2003). "Does aspirin protect against Alzheimer's dementia? A study in a Swedish population-based sample aged > or =80 years". European journal of clinical pharmacology 59 (4): 313–9. doi:10.1007/s00228-003-0618-y. PMID 12827329. 
  18. ^ Anthony, JC; Breitner, JC; Zandi, PP; Meyer, MR; Jurasova, I; Norton, MC; Stone, SV (2000). "Reduced prevalence of AD in users of NSAIDs and H2 receptor antagonists: the Cache County study". Neurology 54 (11): 2066–71. doi:10.1212/wnl.54.11.2066. PMID 10851364. 
  19. ^ Ad2000 Collaborative, Group; Bentham, P; Gray, R; Sellwood, E; Hills, R; Crome, P; Raftery, J (2008). "Aspirin in Alzheimer's disease (AD2000): a randomised open-label trial". Lancet neurology 7 (1): 41–9. doi:10.1016/S1474-4422(07)70293-4. PMID 18068522. 
  20. ^ Akiyama, H; Barger, S; Barnum, S; Bradt, B; Bauer, J; Cole, GM; Cooper, NR; Eikelenboom, P; Emmerling, M (2000). "Inflammation and Alzheimer's disease". Neurobiology of Aging 21 (3): 383–421. doi:10.1016/S0197-4580(00)00124-X. PMID 10858586. 
  21. ^ Tortosa, E; Avila, J; Pérez, M (2006). "Acetylsalicylic acid decreases tau phosphorylation at serine 422". Neuroscience letters 396 (1): 77–80. doi:10.1016/j.neulet.2005.11.066. PMID 16386371. 
  22. ^ Hirohata, M; Ono, K; Naiki, H; Yamada, M (2005). "Non-steroidal anti-inflammatory drugs have anti-amyloidogenic effects for Alzheimer's beta-amyloid fibrils in vitro". Neuropharmacology 49 (7): 1088–99. doi:10.1016/j.neuropharm.2005.07.004. PMID 16125740. 
  23. ^ Thomas, T; Nadackal, TG; Thomas, K (2001). "Aspirin and non-steroidal anti-inflammatory drugs inhibit amyloid-beta aggregation". NeuroReport 12 (15): 3263–7. doi:10.1097/00001756-200110290-00024. PMID 11711868.