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Lack of association between apolipoprotein E genotypes and cognitive performance in the non‐demented elderly
Author(s) -
Quintas Juliana Lima,
Souza Vinícius Carolino,
Henriques Adriane Dallanora,
MachadoSilva Wilcelly,
Toledo Juliana Oliveira,
Córdova Cláudio,
Moraes Clayton Franco,
Camargos Einstein Francisco,
Nóbrega Otávio Toledo
Publication year - 2014
Publication title -
psychogeriatrics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.647
H-Index - 32
eISSN - 1479-8301
pISSN - 1346-3500
DOI - 10.1111/psyg.12029
Subject(s) - dementia , cognition , apolipoprotein e , context (archaeology) , effects of sleep deprivation on cognitive performance , allele , disease , episodic memory , cognitive decline , association (psychology) , psychology , genotype , alzheimer's disease , clinical psychology , medicine , gerontology , psychiatry , genetics , biology , gene , paleontology , psychotherapist
Aim The ε4 alelle of the apolipoprotein E gene is known to be a key genetic risk factor for A lzheimer's disease and possibly for other neurological disorders. Some evidence in the literature indicates that the ε4 allele interferes with human cognition independently of chronological age and diagnosis of A lzheimer's disease. The present study investigated the correlation of allelic variants of apolipoprotein E with the cognitive performance of elderly individuals without apparent cognitive impairment. Methods This was a cross‐sectional analysis that included 213 non‐demented elderly individuals (age ≥60 years) from the B razilian F ederal D istrict. The analysis assessed the subjects for cognitive domains including short‐ and long‐term episodic memory, processing speed, and attention and executive functions. Sociodemographic and other clinical characteristics were gathered and analyzed as covariates. Results Being sufficiently powered, the present study did not identify differential performance across apolipoprotein E genotypes. There was no influence of age, gender, marital status, schooling, depressive symptoms or use of central nervous system depressants when the analyses were controlled for such factors. Conclusions Our findings suggest that the ε4 allele does not contribute to detectable cognitive decline within the context of non‐dementia.