Will testing for apolipoprotein E assist in tailoring dementia risk reduction? A review

• Published in: Neuroscience and biobehavioral reviews Vol. 34; no. 3; pp. 408 - 437
• Main Authors: Low, Lee-Fay, Yap, Melvyn H.W., Brodaty, Henry
• Format: Journal Article
• Language: English
• Published: Kidlington Elsevier Ltd 01.02.2010; Elsevier
• Subjects: Adult and adolescent clinical studies; Alzheimer's disease; Apolipoprotein E; Apolipoproteins E - genetics; Behavioral psychophysiology; Biological and medical sciences; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Dementia; Dementia - diagnosis; Dementia - genetics; Dementia - prevention & control; Fundamental and applied biological sciences. Psychology; Genetic Predisposition to Disease; Gene–environment interactions; Humans; Medical sciences; Neurology; Organic mental disorders. Neuropsychology; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Psychopathology. Psychiatry; Risk Factors; Risk Reduction Behavior; Systematic review; Systematic review; Gene–environment interactions; Apolipoprotein E; Alzheimer's disease; Risk factors; Dementia; Nervous system diseases; Alzheimer disease; Review; Cerebral disorder; Gene-environment interactions; Genotype environment interaction; Central nervous system disease; Risk factor; Degenerative disease
• ISSN: 0149-7634; 1873-7528
• DOI: 10.1016/j.neubiorev.2009.08.007

This paper aims to systematically review the influence of apolipoprotein E (ApoE) on the effects of potentially modifiable mid and late life risk factors for dementia. Scopus, Medline, PubMed, PsycINFO, and HuGE databases were searched up to November 2008. Two independent reviewers selected 94 articles from 13,122 results. Results suggest the deleterious effect of current smoking is limited only to persons without ApoE ɛ4 (4 out of 4 studies), ApoE ɛ4 increases the risk of dementia associated with greater fat consumption, particularly saturated fats (3 out of 4 studies), and increases the protective effect against dementia associated with HRT use (3 out of 5 with one of the non-significant studies suggesting a trend). There was evidence that ApoE does not modify the risk of dementia associated with measures of, and treatments for CVD, other dietary factors, and estradiol levels. There was inconsistent or contradictory evidence for other environmental factors reviewed. There is insufficient evidence for the recommendation of ApoE testing to assist with tailoring risk reduction recommendations for dementia.