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Increased risk of mortality in alzheimer's disease patients with more advanced educational and occupational attainment
Author(s) -
Stern Yaakov,
Tang Ming Xi,
Denaro Jean,
Mayeux Richard
Publication year - 1995
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410370508
Subject(s) - medicine , disease , socioeconomic status , confidence interval , demography , dementia , cognitive reserve , proportional hazards model , educational attainment , alzheimer's disease , relative risk , gerontology , pediatrics , population , economics , economic growth , environmental health , sociology
Abstract A reserve hypothesis suggests that clinical symptoms of Alzheimer's disease (AD) begin earlier in individuals with less education. Therefore, patients with less education might survive longer after diagnosis than those with more education. Two hundred forty‐six subjects with probable AD were following for 1 to 4 years. There were 78 deaths; 30 deaths occurred in the 127 patients whose education was ≤8 years, while 48 deaths occured in the 119 patients with <8 years of education. Cox proportional hazards models adjusted for age, gender, and clinical dementia rating (CDR) showed that patients with more education had increased mortality (continuous variable: RR = 1.06 for each years of education; 95% confidence interval {CI}, 1.01‐1.11; dichotomous variable at 8 yr: RR = 1.76; CI, 1.11‐2.77). This observation might at first seem counterintuitve, since groups with lower socioeconomic status are often at greater mortality risk. It implies that at any level of assessed clinical severity, the underlying pathology of AD is more advanced in patients with more education, resulting in shorter duration of diagnosed disease before death. These findings suggest either that education systematically influences global ratings of disease severity or that education provides a reserve against the clinical manifestation of AD pathology.