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P2‐105: Dendritic and spinal pathology in the visual cortex in Alzheimer's disease
Author(s) -
Baloyannis Stavros
Publication year - 2012
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.2012.05.810
Subject(s) - dendritic spine , pathology , pathological , disease , cortex (anatomy) , visual cortex , neuroscience , medicine , biology , psychology , hippocampal formation
diagnostic markers for Alzheimer disease (AD). Whether a progressive distribution of these neuropathological markers exists in normal cognitive aging, cognitive impairment no dementia (CIND) and AD remains unknown. The relevance of vascular brain lesions for the occurrence of CIND is still unsettled. To address this question, we compared the burden of AD neuropathologic markers and vascular brain lesions in autopsied individuals with CIND and cognitive normal aging. Methods: Charts of deceased individuals older than 50 years of age whose brains had been donated to the Brain Bank of the Brazilian Aging Brain Study Group were examined. The clinical diagnosis was established through a postmortem interview with an informant including the Cognitive Dementia Rating (CDR). Only individuals with a global CDR score of 0 (control group, n 1⁄4 185) and 0.5 (CIND group, n 1⁄4 40) were included. To be included as CDR 0.5, besides the overall rating of 0.5, individuals should have a score of 0.5 or 1 in the memory domain and a score of 0 or 0.5 in the domains of judgment and problem solving, community affairs, home and hobbies, and personal care (in order to exclude individuals with significant functional impairment). All the individuals with severe visual and auditory impairment and active alcoholics were excluded from the study. Neuropathological examinations were carried out based on accepted criteria, using immunohistochemistry. Groups were compared using non-parametric tests followed by adjustment for confounding factors with multivariate logistic regression. Results: NFTs and neuritic plaques were higher (P 1⁄4 0.03 and 0.006, respectively) in the CIND group compared to controls. Both associations remained significant after multivariate logistic regression, adjusting for age, gender and years of education (P 1⁄4 0.006 and 0.002, respectively). Percentage of lacunar infarction was higher in the CIND group (P 1⁄4 0.02), however after multivariate analysis this association disappeared (P 1⁄4 0.12). Percentage of widespread hyaline arteriolosclerosis and cerebral amyloid angiopathy was similar between groups (P 1⁄4 0.07 and 0.80, respectively). Conclusions: CIND showed a higher burden of AD changes than controls, whereas no significant changes were found for vascular related lesions. From a neuropathologic perspective, CIND is best interpreted as a stage between normal cognitive aging and AD.