Abstracts on niacin, statin drugs and coffee having a protective effecta against Alzheimer's Disease
J Neurol Neurosurg Psychiatry. 2004 Aug;75(8):1093-9.
Dietary niacin and the risk of incident Alzheimer's disease and of cognitive decline.
Morris MC, Evans DA, Bienias JL, Scherr PA, Tangney CC, Hebert LE, Bennett DA, Wilson RS, Aggarwal N.
Rush Institute for Healthy Aging, Centers for Disease Control and Prevention, Atlanta , GA , USA . email@example.com
BACKGROUND: Dementia can be caused by severe niacin insufficiency, but it is unknown whether variation in intake of niacin in the usual diet is linked to neurodegenerative decline. We examined whether dietary intake of niacin was associated with incident Alzheimer's disease (AD) and cognitive decline in a large, prospective study. METHODS: This study was conducted in 1993-2002 in a geographically defined Chicago community of 6158 residents aged 65 years and older. Nutrient intake was determined by food frequency questionnaire. Four cognitive tests were administered to all study participants at 3 year intervals in a 6 year follow up. A total of 3718 participants had dietary data and at least two cognitive assessments for analyses of cognitive change over a median 5.5 years. Clinical evaluations were performed on a stratified random sample of 815 participants initially unaffected by AD, and 131 participants were diagnosed with 4 year incident AD by standardised criteria. RESULTS: Energy adjusted niacin intake had a protective effect on development of AD and cognitive decline. In a logistic regression model, relative risks (95% confidence intervals) for incident AD from lowest to highest quintiles of total niacin intake were: 1.0 (referent) 0.3 (0.1 to 0.6), 0.3 (0.1 to 0.7), 0.6 (0.3 to 1.3), and 0.3 (0.1 to 0.7) adjusted for age, sex, race, education, and ApoE e4 status. Niacin intake from foods was also inversely associated with AD (p for linear trend = 0.002 in the adjusted model). In an adjusted random effects model, higher food intake of niacin was associated with a slower annual rate of cognitive decline, by 0.019 standardised units (SU) per natural log increase in intake (mg) (p = 0.05). Stronger associations were observed in analyses that excluded participants with a history of cardiovascular disease (beta = 0.028 SU/year; p = 0.008), those with low baseline cognitive scores (beta = 0.023 SU/year; p = 0.02), or those with fewer than 12 years' education (beta = 0.035 SU/year; p = 0.002) CONCLUSION: Dietary niacin may protect against AD and age related cognitive decline.
PMID: 15258207 [PubMed - indexed for MEDLINE]
J Clin Pharm Ther. 2004 Jun;29(3):209-13.
Do statins slow down Alzheimer's disease? A review.
Caballero J, Nahata M.
The Ohio State University , Columbus , OH 43210 , USA .
More than 4 million people suffer from Alzheimer's disease (AD) in the United States . The prevalence increases with age as the rate is 3% in those between 65 and 74 years compared with 47% among those over 85 years of age. Some epidemiological studies have reported a decrease in the incidence of AD with the use of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins). Other studies have shown statins to decrease Abeta peptides, but data regarding cognitive benefits is lacking in this patient population. There are also concerns that statins, which cross the blood-brain barrier may cause more side-effects, but more information is needed. Adverse events were either infrequently noted or not reported in most of the published studies, and at this time there is insufficient evidence to suggest the use of statins for cognitive improvements in patients with AD.
PMID: 15153082 [PubMed - in process]
Arch Neurol. 2003 Apr;60(4):510-5.
Reduction in levels of 24S-hydroxycholesterol by statin treatment in patients with Alzheimer disease.
Vega GL, Weiner MF, Lipton AM, Von Bergmann K, Lutjohann D, Moore C, Svetlik D.
Department of Clinical Nutrition, the Center for Human Nutrition, University of Texas Southwestern Medical Center and Nutrition and Metabolism Laboratory, Veterans Affairs Medical Center, Dallas 75390, USA. Gloria.Vega@utsouthwestern.edu
BACKGROUND: The statin treatment of dyslipidemia is associated with a reduced risk of development of Alzheimer disease (AD). The effect may be mediated by a reduction in cholesterol biosynthesis in the brain, by lowering levels of apolipoprotein E (apo E)-containing lipoproteins, or by pleitropic effects such as reduction in beta-amyloid production. In the brain, cholesterol from damaged or dying neurons is converted to 24S-hydroxycholesterol by cholesterol 24-hydroxylase (CYP46). The oxysterol is subsequently transferred across the blood-brain barrier, transported to the liver by low-density lipoproteins (LDLs), and excreted as bile acids. Most of plasma 24S-hydroxycholesterol is derived from brain cholesterol; consequently, plasma levels of the oxysterol reflect brain cholesterol catabolism. OBJECTIVE: To examine the effect of 3 statins and a nonstatin hypolipidemic agent on plasma levels of 24S-hydroxycholesterol and apo E in patients with AD. STUDY DESIGN: The study had a sequential parallel design. It was open-labeled and involved lipoprotein and 24S-hydroxycholesterol evaluations at baseline and at 6 weeks of treatment with 40 mg of lovastatin, simvastatin, or pravastatin sodium per day, or 1 g of extended-release niacin per day. Blood samples were drawn after a 12-hour fast for measurement of plasma sterols, oxysterols, lipoprotein cholesterol, and levels of apo E, plasma transaminases, and glucose. Measurements were made at baseline and during treatment. RESULTS: Statin treatment reduced levels of plasma lathosterol by 49.5%, 24S-hydroxycholesterol by 21.4%, LDL cholesterol by 34.9%, and total cholesterol by 25%. The ratios of lathosterol-campesterol and 24S-hydroxycholesterol-LDL cholesterol were reduced significantly, but the ratio of 24S-hydroxycholesterol-total cholesterol was unchanged. Extended-release niacin also significantly reduced levels of 24S-hydroxycholesterol by 10% and LDL cholesterol by 18.1%. None of the agents lowered plasma concentration of apo E. CONCLUSIONS: Statins lowered levels of plasma 24S-hydroxycholesterol without affecting levels of apo E. The LDL lowering was more pronounced than 24S-hydroxycholesterol reductions. The effect of statins on LDL partially explains the reduction of plasma oxysterol level.
PMID: 12707064 [PubMed - indexed for MEDLINE]
Am J Epidemiol. 2002 Sep 1;156(5):445-53.
Risk factors for Alzheimer's disease: a prospective analysis from the Canadian Study of Health and Aging.
Lindsay J, Laurin D, Verreault R, Hebert R, Helliwell B, Hill GB, McDowell I.
Department of Epidemiology and Community Medicine, Faculty of Medicine, University of Ottawa , Ottawa , ON , Canada . Joan_Lindsay@hc-sc.gc.ca
A prospective analysis of risk factors for Alzheimer's disease was a major objective of the Canadian Study of Health and Aging, a nationwide, population-based study. Of 6,434 eligible subjects aged 65 years or older in 1991, 4,615 were alive in 1996 and participated in the follow-up study. All participants were cognitively normal in 1991 when they completed a risk factor questionnaire. Their cognitive status was reassessed 5 years later by using a similar two-phase procedure, including a screening interview, followed by a clinical examination when indicated. The analysis included 194 Alzheimer's disease cases and 3,894 cognitively normal controls. Increasing age, fewer years of education, and the apolipoprotein E epsilon4 allele were significantly associated with increased risk of Alzheimer's disease. Use of nonsteroidal anti-inflammatory drugs, wine consumption, coffee consumption, and regular physical activity were associated with a reduced risk of Alzheimer's disease. No statistically significant association was found for family history of dementia, sex, history of depression, estrogen replacement therapy, head trauma, antiperspirant or antacid use, smoking, high blood pressure, heart disease, or stroke. The protective associations warrant further study. In particular, regular physical activity could be an important component of a preventive strategy against Alzheimer's disease and many other conditions.
• Multicenter Study
PMID: 12196314 [PubMed - indexed for MEDLINE]