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Commentary on “Vascular cognitive impairment: Today and tomorrow”
Author(s) -
Bennett David A.
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.2006.04.009
Subject(s) - gold rush , cognitive impairment , citation , center (category theory) , gerontology , library science , psychology , medicine , history , cognition , computer science , psychiatry , chemistry , archaeology , crystallography
b r t i i a N e D p c r c Loss of cognitive abilities in old age has been recognized or more than 4,000 years. However, the clinical description f dementia was not established in the medical literature ntil the late 18th century. By the mid to late 19th century, he term senile dementia was being used to differentiate the ore common age-related dementia from dementia in oung and middle-aged persons, although little was known bout the underlying neuropathology of these conditions. y the late 19th century, progress in neuropathologic methds including brain tissue fixation, tissue staining, and imroved microscope optics markedly enhanced the ability of euroscientists to examine postmortem brain tissue from umans. This set the stage for clinical–pathologic case studes to inform our understanding of neuropathology of deentia and other neurologic conditions. The role of cererovascular disease as a contributor to dementia was mmediately apparent. In 1894, Otto Binswanger described clinical–pathologic syndrome of chronic progressive subortical encephalitis that would eventually be named inswanger’s disease [1,2]. In 1898, Alois Alzheimer decribed senile cortical atrophy, which he thought was caused y arteriosclerosis [3]. This was nearly a decade before the ase report of Augusta D, which described a clinical–pathoogic syndrome of progressive dementia in midlife not vasular in origin that would eventually be named Alzheimer’s isease (AD) [4]. For the next 6 decades, AD was thought o be a relatively obscure disease causing progressive deentia in midlife and something distinct from the all too ommon age-related senility that was considered to be the esult of arteriosclerosis or “hardening of the arteries.” By the middle of the 20th century, case series were slowly eplacing single case studies as a means of investigating the eurobiology of senile dementia. In a seminal series of papers, omlinson, Blessed, and Roth firmly established a role for oth cerebrovascular disease, especially in the form of large nd multiple gross cerebral infarctions, and ad pathology, in