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AD lesions and infarcts in demented and non‐demented Japanese‐American men
Author(s) -
Petrovitch Helen,
Ross G. Webster,
Steinhorn Sandra C.,
Abbott Robert D.,
Markesbery William,
Davis Daron,
Nelson James,
Hardman John,
Masaki Kamal,
Vogt Margaret R.,
Launer Lenore,
White Lon R.
Publication year - 2005
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.20318
Subject(s) - dementia , senile plaques , alzheimer's disease , medicine , lesion , pathology , psychology , cardiology , disease
Neocortical neuritic plaques and neurofibrillary tangles are hallmark neuropathological lesions of dementia. Concomitant cerebrovascular lesions increase dementia severity in patients meeting neuropathological criteria for Alzheimer's disease and contribute to cognitive impairment in persons with mild entorhinal Alzheimer lesions. This study investigates whether individuals with sparse neocortical neuritic plaques experience increased odds of crossing the threshold to clinical dementia when they have coexistent cerebrovascular lesions. Dementia examinations were given to 3,734 men during the 1991–1993 Honolulu‐Asia Aging Study examination and to 2,603 men during the 1994–1996 examination. Lesion quantification was done without clinical data. Among 333 autopsied men, 120 had dementia, 115 had marginal results, and 98 had normal cognition. In men with neurofibrillary tangles, dementia frequency increased with increasing neuritic plaque density, and increased further in the presence of cerebrovascular lesions. The association was strongest in men with sparse neuritic plaques (1–3/mm 2 ) where dementia frequency more than doubled with coexistent cerebrovascular lesions (45 vs 20%). Among all dementia cases, 24% were linked to cerebrovascular lesions. Findings suggest cerebrovascular lesions are associated with a marked excess of dementia in cases with low neuritic plaque frequency. Prevention of cerebrovascular lesions may be critically important in preserving late‐life cognitive function. Ann Neurol 2005