Prevention of dementia

Prevention of dementia is the attempt to avoid developing dementia. Although no cure for dementia is available, there are ways of decreasing the risk of developing dementia, including both lifestyle changes and medication.

Efforts to prevent dementia include trying to decrease risk factors for vascular disease, including diabetes, high blood pressure, obesity, smoking and physical inactivity.[1]

Lifestyle

Mental activity

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, learning a new language, 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.[2] [3] The risk decrease is proportional to frequency of activity,[2] with slower cognitive decline being associated with both late-life and early-life increased cognitive activity.[4]

SMART Brain Aging is a cognitive rehabilitation program designed to improve brain function in elderly individuals who may have early memory loss, including Mild Cognitive Impairment MCI. The treatment was developed by Scottsdale, Arizona-based Clinical Neuropsychologist John DenBoer. This early stage dementia treatment has received media attention due to the positive results patients are experiencing as a result of the SMART Brain Aging Program.[5] DenBoer is part of a growing community of neuropsychologists who believe regimented and personalized mental exercises can help slow the progress of dementia significantly.

Apart from spare time activities, a mentally demanding job may prevent dementia, especially during the thirties, forties and fifties.[2]

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.[2]

Physical activity

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.[2] An active lifestyle can almost halve the risk compared to a sedentary one.[2]

The effect of physical activity is not limited to vascular effects. Physical activity can give rise to new neurons in the brain, as well as releasing a substance that can protect them.[2] 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.[6]

Some studies say Alzheimer's and other dementias may be caused by high blood pressure, since it can cause blood vessel damage through constriction.[7][8]

Diet

Obesity increases the risk of any dementia and Alzheimer's disease in particular.[2] The effect of alcohol on the risk of dementia is a J curve:[9] high alcohol consumption increases the risk of dementia[10] while low alcohol consumption may be protective.[9][11] However, low alcohol consumption may not protect against vascular dementia and overall cognitive decline.[9] 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.[12]

The effects of omega-3 fatty acid in the prevention of dementia is uncertain.[13] Vegetables and nuts may be of benefit,[2] because of their high content of polyunsaturated fats. Non-fish meat, on the other hand, increases the risk of Alzheimer's,[2] 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.

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.[12]

There is evidence for an association between cognitive decline, homocysteine (Hcy) status, and vitamin B status relating especially to B12[14] and also to vitamins B6 and B9.[15] In particular, deficiency of vitamin B12 and/or of folate can cause an increase in Hcy plasma levels, which in turn leads to toxic effects on the vascular and nervous systems.[16]

Vitamin D deficiency correlates with cognitive impairment and dementia; however, the value of vitamin D substitution in cognitive impairment remains doubtful.[17][18][19]

Sleep pattern

More than nine hours of sleep per day (including daytime napping) may be associated with an increased risk of dementia.[20] Lack of sleep may also increase risk of dementia by increasing beta-amyloid deposition.[21]

Personality and Mental Health

Being neurotic increases the risk of developing Alzheimer's, a type of dementia.[22][23] Neuroticism is associated with increased brain atrophy and cognitive impairment in life, while conscientiousness has a protective effect by preventing brain atrophy.[24]

Medication

Hypertension medications

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.[25]

Anti-diabetic drugs

Diabetes mellitus is a risk factor for vascular dementia, and is thus the risk is lowered with anti-diabetic drugs.[26]

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.[2] Thus, less insulin needs to be released to achieve its metabolic effects. Insulin in the bloodstream is a trigger of amyloid beta-production,[26][27] so decreased insulin levels decrease the level of amyloid beta. This leads to less formation of amyloid plaques seen in Alzheimer's disease.

Steroid hormones

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.[28] Recent evidence on the effects of estrogen do not allow for an unambiguous recommendation for estrogen supplementation and they indicate that the timing of estrogen supplementation may be important, with early postmenopausal use being preferable over its use later in life.[29][30]

NSAIDs

Non-steroidal anti-inflammatory drugs (NSAIDs) can decrease the risk of developing Alzheimer's and Parkinson's diseases.[2] The length of time needed to prevent dementia varies, but in most studies it is usually between 2 and 10 years.[31][32][33][34][35] 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.[36]

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.[37] NSAIDs inhibit the formation of such inflammatory substances, and prevent the deteriorating effects.[38][39][40]

Vaccine

There is as yet no vaccine against dementia.[2] It has been theorized that 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.[2]

See also

References

  1. ↑ "WHO Media centre fact sheets: Dementia. Fact sheet N°362". April 2012. Retrieved 21 January 2015.
  2. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 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.
  3. ↑ "Bilingualism delays age at onset of dementia, independent of education and immigration status". Neurology. Published online before print. 2013-11-06.
  4. ↑ Wilson, Robert S.; et al. (3 July 2013). "Life-span cognitive activity, neuropathologic burden, and cognitive aging (Abstract)". Neurology. Archived from the original on 5 July 2013. Explained by Koren, Marina (23 July 2013). "Being a Lifelong Bookworm May Keep You Sharp in Old Age". Smithsonian. Archived from the original on 5 July 2013.
  5. ↑ http://finance.boston.com/boston/news/read/31803993/
  6. ↑ Jones, Hilary. "Dr". http://www.telecare24.co.uk/blog/dr-hilary-jones-preventing-dementia-exercise/. External link in |website= (help);
  7. ↑ "Blood pressure drug dementia hope". BBC News. 28 July 2008. Retrieved 2 October 2009.
  8. ↑ "Blood Pressure Drugs May Protect Against Alzheimer's" (Press release). Boston University School of Medicine. 27 July 2008. Retrieved 2 October 2009.
  9. 1 2 3 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.
  10. ↑ 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.
  11. ↑ Peters R, Peters J, Warner J, Beckett N, Bulpitt C (2008). "Alcohol, dementia and cognitive decline in the elderly: a systematic review". Age and Ageing. 37 (5): 505–12. doi:10.1093/ageing/afn095. PMID 18487267.
  12. 1 2 Robert, Levine (2006). "Defying dementia: understanding and preventing Alzheimer's and related disorders". Westport: conn: Praeger.
  13. ↑ 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.
  14. ↑ Gröber U, Kisters K, Schmidt J (2013). "Neuroenhancement with vitamin B12-underestimated neurological significance". Nutrients (Review). 5 (12): 5031–45. doi:10.3390/nu5125031. PMC 3875920Freely accessible. PMID 24352086.
  15. ↑ Reay JL, Smith MA, Riby LM (2013). "B vitamins and cognitive performance in older adults: review". ISRN Nutrition (Review). 2013: 650983. doi:10.5402/2013/650983. PMC 4045270Freely accessible. PMID 24959550.
  16. ↑ Ansari R, Mahta A, Mallack E, Luo JJ (2014). "Hyperhomocysteinemia and neurologic disorders: a review". Journal of Clinical Neurology (Seoul, Korea) (Review). 10 (4): 281–8. doi:10.3988/jcn.2014.10.4.281. PMC 4198708Freely accessible. PMID 25324876.
  17. ↑ Schlögl M, Holick MF (2014). "Vitamin D and neurocognitive function". Clinical Interventions in Aging (Review). 9: 559–68. doi:10.2147/CIA.S51785. PMC 3979692Freely accessible. PMID 24729696.
  18. ↑ Etgen T, Sander D, Bickel H, Sander K, Förstl H (2012). "Vitamin D deficiency, cognitive impairment and dementia: a systematic review and meta-analysis". Dementia and Geriatric Cognitive Disorders (Review). 33 (5): 297–305. doi:10.1159/000339702. PMID 22759681.
  19. ↑ Dickens AP, Lang IA, Langa KM, Kos K, Llewellyn DJ (2011). "Vitamin D, cognitive dysfunction and dementia in older adults". CNS Drugs. 25 (8): 629–39. doi:10.2165/11593080-000000000-00000. PMID 21790207.
  20. ↑ 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.
  21. ↑ "Lack of sleep may increase Alzheimer's risk". Medical News Today. Retrieved 21 March 2016.
  22. ↑ http://www.alzheimersresearchuk.org/news-detail/11160/Neuroticism-and-other-personality-traits-in-midlife-linked-to-Alzheimers-risk/
  23. ↑ , http://www.webmd.com/women/news/20141001/jealous-moody-women-may-face-higher-alzheimers-risk-study-says
  24. ↑ "Exploring the relationship between personality and regional brain volume in healthy aging". PubMed Central (PMC). Retrieved 21 March 2016.
  25. ↑ 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.
  26. 1 2 "Diabetes and Alzheimer's linked" (Press release). Mayo Clinic. 6 November 2008. Retrieved 2 October 2009.
  27. ↑ "Obesity Today, Alzheimer's Disease Tomorrow?". WebMD. Retrieved 21 March 2016.
  28. ↑ Eileen M., Welsh (2003). "Focus on Alzheimer's disease research". Nova Biomedical books: 699.
  29. ↑ Simpkins JW, Perez E, Wang X, Yang S, Wen Y, Singh M (2009). "The potential for estrogens in preventing Alzheimer's disease and vascular dementia". Therapeutic Advances in Neurological Disorders. 2 (1): 31–49. doi:10.1177/1756285608100427. PMC 2771945Freely accessible. PMID 19890493.
  30. ↑ Anderson P (25 October 2012). "Timing of Hormone Therapy May Affect Alzheimer's Prevention". Medscape.
  31. ↑ 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 2755238Freely accessible. PMID 18509093.
  32. ↑ 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.
  33. ↑ 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 165707Freely accessible. PMID 12869452.
  34. ↑ 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.
  35. ↑ 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.
  36. ↑ 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.
  37. ↑ 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.
  38. ↑ 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.
  39. ↑ 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.
  40. ↑ 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.
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