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IC–P–062: Prevalence and risk factors of cerebral microbleeds in the Rotterdam scan study
Author(s) -
Vernooij Meike W.,
Lugt Aad,
Ikram Mohammad A.,
Wielopolski Piotr,
Hofman Albert,
Krestin Gabriel P.,
Breteler Monique M.
Publication year - 2006
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.2006.05.2267
Subject(s) - medicine , cerebral amyloid angiopathy , rotterdam study , logistic regression , cohort , magnetic resonance imaging , grey matter , population , confounding , cohort study , white matter , radiology , disease , dementia , environmental health
ries. Methods: The sample at risk was 1554 Japanese-American old men without dementia and who were cognitively intact at a baseline exam (199193) of the Honolulu-Asia Aging Study. All participants returned to two follow up exams (1994-96 and 1997-99). Among this group, 156 autopsies were obtained between April 1992 and March 2005. Dementia cases were diagnosed by international criteria. We defined subjects as “cognitively impaired, not demented” (CIND) based on both a CASI score (60 to 81.9) and a CDR (0.5). Subjects were divided into 4 groups based on their trajectories of cognitive decline from the baseline exam to the subsequent exams: 1) Subjects who were cognitively intact during the entire period (Normal); 2) subjects who declined to CIND but did not develop dementia (CIND-only); 3) subjects who declined to CIND at the first follow up exam and developed dementia at the second follow up (CIND-Dem); and 4) subjects who developed dementia without first developing CIND during the follow up period (Rapid). Results and Conclusions: The frequency of APOE4 allele declined significantly across the Rapid, CIND-Dem, CIND only, and Normal, groups. Low total CASI score at the baseline predicted the greatest cognitive decline in the course of follow-up. Episodic memory, concentration/mental manipulation, and list-generating fluency were significantly lower at baseline in subjects who later developed dementia. The frequencies of several of the neuropathologic findings, including Braak stages 5 and 6, probable/definite AD by CERAD neuropathologic criteria, moderate/high density of Alzheimer lesions, moderate/high density of cortical Lewy bodies, and levels of gliosis/neuronal loss in the substantia nigra, locus ceruleus and hippocampus became more apparent in groups with greater cognitive decline. The CIND-only group had less neuropathologic findings than either of the groups that developed dementia. There was no significant difference across the groups in brain volume loss, frequencies of microvascular lesions, hippocampal sclerosis, or cerebral amyloid angiopathy. Our findings may help to understand predominant pathologies contributing to rapid cognitive decline.