Document Detail

Dietary fatty acids in dementia and predementia syndromes: epidemiological evidence and possible underlying mechanisms.
MedLine Citation:
PMID:  19643207     Owner:  NLM     Status:  MEDLINE    
Drugs currently used in the treatment of cognitive impairment and dementia have a very limited therapeutic value, suggesting the necessity to potentially individualize new strategies able to prevent and to slow down the progression of predementia and dementia syndromes. An increasing body of epidemiological evidence suggested that elevated saturated fatty acids (SFA) could have negative effects on age-related cognitive decline (ARCD) and mild cognitive impairment (MCI). Furthermore, a clear reduction of risk for cognitive decline has been found in population samples with elevated fish consumption, high intake of monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUFA), particularly n-3 PUFA. Epidemiological findings demonstrated that high PUFA intake appeared to have borderline non-significant trend for a protective effect against the development of MCI. Several hypotheses could explain the association between dietary unsaturated fatty acids and cognitive functioning, including mechanisms through the co-presence of antioxidant compounds in food groups rich in fatty acids, via atherosclerosis and thrombosis, inflammation, accumulation of b-amyloid, or via an effect in maintaining the structural integrity of neuronal membranes, determining the fluidity of synaptosomal membranes that thereby regulate neuronal transmission. However, recent findings from clinical trials with n-3 PUFA supplementation showed efficacy on depressive symptoms only in non-apolipoprotein E (APOE) epsilon4 carriers, and on cognitive symptoms only in very mild Alzheimer's disease (AD) subgroups, MCI patients, and cognitively unimpaired subjects non-APOE epsilon4 carriers. These data together with epidemiological evidence support a possible role of fatty acid intake in maintaining adequate cognitive functioning and possibly for the prevention and management of cognitive decline and dementia, but not when the AD process has already taken over.
Vincenzo Solfrizzi; Vincenza Frisardi; Cristiano Capurso; Alessia D'Introno; Anna M Colacicco; Gianluigi Vendemiale; Antonio Capurso; Francesco Panza
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2009-07-28
Journal Detail:
Title:  Ageing research reviews     Volume:  9     ISSN:  1872-9649     ISO Abbreviation:  Ageing Res. Rev.     Publication Date:  2010 Apr 
Date Detail:
Created Date:  2010-03-15     Completed Date:  2010-06-15     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101128963     Medline TA:  Ageing Res Rev     Country:  England    
Other Details:
Languages:  eng     Pagination:  184-99     Citation Subset:  IM    
Copyright Information:
Copyright 2009 Elsevier Ireland Ltd. All rights reserved.
Department of Geriatrics, Center for Aging Brain, Memory Unit, University of Bari, Policlinico, Piazza Giulio Cesare, 11, 70124 Bari, Italy.
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MeSH Terms
Aging / metabolism*
Apolipoprotein E4 / genetics,  metabolism
Brain / metabolism*,  physiopathology
Cognition Disorders / epidemiology,  metabolism*,  physiopathology
Dementia / epidemiology,  metabolism*,  physiopathology
Dietary Fats / metabolism*
Disease Progression
Fatty Acids / metabolism*
Fatty Acids, Unsaturated / metabolism
Lipid Metabolism / physiology*
Risk Factors
Reg. No./Substance:
0/Apolipoprotein E4; 0/Dietary Fats; 0/Fatty Acids; 0/Fatty Acids, Unsaturated

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