The role of nutrients in the prevention and treatment of Alzheimer’s disease: methodology for a systematic review
ABSTRACT There is a large body of existing data on nutrition in Alzheimer's disease (AD). We are conducting a systematic review of published scientific literature to determine the role of specific nutrients, both individually and in combination, in the prevention and treatment of AD. This will contribute towards a structured evidence base to help inform the clinical management of AD. The objective of the systematic review is to evaluate the strength of evidence from both observational cohort studies and randomized controlled trials on the role of fats, vitamins, antioxidants and other nutrients in the prevention and treatment of AD. We present here the methodology of our systematic review.
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ABSTRACT: The increasing worldwide prevalence of dementia is a major public health concern. Findings from some epidemiological studies suggest that diet and nutrition may be important modifiable risk factors for development of dementia. In order to evaluate the strength of the available evidence of an association of dietary factors with dementia including Alzheimer's disease (AD), we systematically searched relevant publication databases and hand-searched bibliographies up to end July 2007. We included prospective cohort studies which evaluated the association of nutrient levels with the risk of developing dementia and randomized intervention studies examining the treatment effect of nutrient supplementation on cognitive function. One hundred and sixty studies, comprising ninety one prospective cohort studies and sixty nine intervention studies, met the pre-specified inclusion criteria. Of these, thirty-three studies (19 cohort and 14 randomized controlled trials) investigated the effects of folate, B-vitamins, and levels of homocysteine (a biomarker modifiable through B-vitamin supplementation) or fish/fatty acids and are the focus of the present report. Some observational cohort studies indicated that higher dietary intake or elevated serum levels of folate and fish/fatty acids and low serum levels of homocysteine were associated with a reduced risk of incident AD and dementia, while other studies reported no association. The results of intervention studies examining the effects of folic acid or fatty acid supplementation on cognitive function are inconsistent. In summary, the available evidence is insufficient to draw definitive conclusions on the association of B vitamins and fatty acids with cognitive decline or dementia, and further long-term trials are required.Journal of Alzheimer's disease: JAD 01/2010; 22(1):205-24. DOI:10.3233/JAD-2010-090940 · 4.15 Impact Factor
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ABSTRACT: Melatonin secretion decreases in Alzheimer´s disease (AD) and this decrease has been postulated as responsible for the circadian disorganization, decrease in sleep efficiency and impaired cognitive function seen in those patients. Half of severely ill AD patients develop chronobiological day-night rhythm disturbances like an agitated behavior during the evening hours (so-called "sundowning"). Melatonin replacement has been shown effective to treat sundowning and other sleep wake disorders in AD patients. The antioxidant, mitochondrial and antiamyloidogenic effects of melatonin indicate its potentiality to interfere with the onset of the disease. This is of particularly importance in mild cognitive impairment (MCI), an etiologically heterogeneous syndrome that precedes dementia. The aim of this manuscript was to assess published evidence of the efficacy of melatonin to treat AD and MCI patients. PubMed was searched using Entrez for articles including clinical trials and published up to 15 January 2010. Search terms were "Alzheimer" and "melatonin". Full publications were obtained and references were checked for additional material where appropriate. Only clinical studies with empirical treatment data were reviewed. The analysis of published evidence made it possible to postulate melatonin as a useful ad-on therapeutic tool in MCI. In the case of AD, larger randomized controlled trials are necessary to yield evidence of effectiveness (i.e. clinical and subjective relevance) before melatonin´s use can be advocated.DNA research: an international journal for rapid publication of reports on genes and genomes 09/2010; 8(3):218-27. DOI:10.2174/157015910792246209 · 2.35 Impact Factor
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ABSTRACT: The formation of the first Gerontopole in Toulouse was a response to a mission letter sent by French Ministers of Health on February 2007. The mission of the Toulouse Gerontopole is based around three major axes: 1) To facilitate the access of frail elderly people to innovative therapy and clinical research: the Gérontopôle set up the national network for clinical investigation into Alzheimer's disease (AD) funded through the CeNGEPS (National Centre For Management of Trials on Health Products) calls for proposals since July 2008. In addition, the Gérontopôle coordinates several national clinical trials with promising drugs with potential effect on the mechanisms and evolution of AD and actively participates in studies on biomarkers; 2) To develop health promotion actions and prevention trials for healthy elderly people, through the Institute of Aging: the Gérontopôle has implemented the GuidAge (Phase III trial concerning the efficiency of Ginkgo Biloba on the impact and delay of appearance of an Alzheimer type dementia) and MAPT (Multi-domain Alzheimer Preventive Trial) studies on prevention of AD and cognitive decline. It is curently working on the new generation of preventive trials based on biomarkers; 3) To develop clinical research for dependant elderly people, through the implementation of the REHPA research network including 240 nursing homes in France. In December 2009, additional grants were delivered by the French government to extend the three research axes for two more years, and establish a charter of quality for geriatric care in relation with the administration and relevant agencies.Journal of Alzheimer's disease: JAD 01/2012; 28(3):721-32. DOI:10.3233/JAD-2011-112202 · 4.15 Impact Factor