How is dementia prevented?

Updated: Sep 19, 2018
  • Author: Richard D Shin, MD; Chief Editor: Gil Z Shlamovitz, MD, FACEP  more...
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Various substances to prevent or retard the onset of dementia have been proposed and/or studied. Prevention mechanisms have included preservation of CNS supporting cells, prevention of CNS inflammation, or free-radical inhibition. Unfortunately, no supplement or medication has been conclusively shown to prevent or retard the progression of dementia.

  • Nonsteroidal anti-inflammatory drugs (NSAIDs): The mechanism of action is thought to involve prevention of CNS inflammation. [20] More recent studies suggest that heavy NSAID intake is a risk factor for dementia; however, moderate intake may delay but not prevent dementia onset. [21]

  • Vitamin E: The suggested dose for prevention is 200-400 IU/d; much higher doses are sometimes given for treatment. The mechanism of action may be antioxidant, free-radical inhibition. Efficacy is controversial and vitamin E can increase mortality risk. Therefore, should only be considered for patients with AD or at high risk for AD.

  • Vitamin B-6, vitamin B-12, and folate: These reduce levels of homocysteine, a potential brain neurotoxin. Efficacy is controversial and recent studies show no benefit.

  • Statin cholesterol-lowering medications: Reports suggest that these drugs substantially protect against dementia via an effect not related directly to blood levels of cholesterol. Mechanisms of action may be reduction of insulin levels in the brain and/or C-reactive protein (CRP) levels in the blood (indicative of inflammation). A study of more than 17,000 adults older than 60 years in Finland concluded that statins appeared to reduce risk by 58%. [22] Other studies have found no benefit to statins in delaying dementia progression in patients with AD.

  • Estrogen replacement: This is being studied, but no evidence of benefit has been found at present.

  • Ginko biloba: This is a medicinal herb considered safe but of questionable efficacy. Preparations are of uncertain purity and dose consistency.

  • High caloric intake in concert with obesity and sedentariness is associated with an increased risk of Alzheimer disease.

Undertreated depression, hypertension, diabetes mellitus, hypercholesterolemia and obesity have all been associated with higher risk of Alzheimer disease.

Excessive amounts of alcohol act as a neurotoxin and can increase Alzheimer disease risk. In moderate doses, alcohol inhibits cerebrovascular disease although it may still enhance brain atrophy. However, recent studies suggest that moderate drinking is protective against dementia as compared with abstinence. Antioxidants in wine (bioflavonoids) may be additionally beneficial (over spirits and beer).

Sedentary lifestyle is an independent risk factor for dementia. Regular exercise is protective.

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