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P3‐332: TEMPORAL LOBE ACTIVATION MODERATES THE DETRIMENTAL EFFECT OF HIPPOCAMPAL ATROPHY ON EPISODIC MEMORY AND CONTRIBUTES TO COGNITIVE RESERVE: RESULTS FROM THE CIMA‐Q COHORT
Author(s) -
Belleville Sylvie,
Mellah Samira,
Cloutier Simon,
Duchesne Simon,
Hudon Carol
Publication year - 2018
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2018.06.1693
Subject(s) - cognitive reserve , psychology , cognition , functional magnetic resonance imaging , temporal lobe , episodic memory , atrophy , hippocampal formation , audiology , neuroscience , medicine , cognitive impairment , epilepsy
greater aging-related decline than persons reporting modest levels of consumption. One recent report even suggested moderately high levels of intake were associated with better cognitive function later in life. We use the HAAS cohort to investigate this association in Japanese-American men. Methods: Alcohol exposure was assess at four time points between 1965 and 1993 (on subject ages 45-93 years). Cognition was assessed every two to three years from 1991 to 2010, using a validated global assessment scale, the Cognitive Abilities Screening Instrument (CASI). Cox proportional hazards regression was used to model risk of moderate cognitive impairment, defined as reaching a score of 74 or less on the CASI. Models were stratified on birth cohort year and covaried for education, APOE e4 status, stroke history, and midlife smoking, BMI, and hypertension. Using the abstinent group as reference, hazard ratios (HR) for cognitive impairment were calculated for six categories of midlife ethyl alcohol exposures, from greater than zero to 100 ounces/month in steps of 20 ounces, and greater than 100 ounces. Results:Of 2,338 persons with exposure data and longitudinal cognitive assessments, a total of 1051 persons crossed the moderate impairment CASI threshold of 74. In Cox models there was no evidence of reduced risk in persons drinking less than 20 ounces/month (HR 1⁄4 1.01, p1⁄40.91). Persons drinking between 20 and 40 ounces/month had increased risk (HR 1⁄4 1.28, p1⁄40.02), and risk steadily increased with each category of increasing consumption. Persons drinking more than 100 ounces/month had HR1⁄42.60-fold higher instantaneous risk of crossing the moderately impaired cognitive function threshold (p 1⁄4 0.004). Conclusions: In the HAAS cohort, there was no evidence of a protective effect of low level consumption, and consistent evidence of a deleterious effect of moderate alcohol consumption on later life cognitive function. Further investigation is required to determine whether these relationships are mediated by specific environmental or health-related exposures and whether specific brain lesions associate with alcohol-related cognitive outcomes.