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Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,6
Jellinger K. A.
Institute of Clinical Neurobiology, Vienna, Austria
The prevalence, morphology, and pathogenesis of vascular dementia (VaD), recently termed vascular cognitive impairment (VCI), and of mixed dementia (Alzheimer disease associated with vascular encephalopathy) are a matter of discussion and clinical diagnostic criteria for these disorders slow low sensitivity and variable specificty. In Western memory clinic-based series, VaD/VCI is suggested in 8-10% of cognitively impaired elderly subjects. Its prevalence in autopsy series ranges from 0.03% to 58% with reasonable values of 4-10%. It has been related to focal, multifocal or diffuse cortical and/or subcortical microinfarcts and lacunes often affecting strategically important brain areas (thalamus, frontobasal and/or limbic systems), hemispheric white matter lesions and, less often, large brain infarcts. They result from systemic, cardiac or local large or small vessel disease. The pathogenesis of cerebrovascular lesions is multifactorial and their pathophysiology affects neuronal systems involved in cognition, memory, and behavior. Vascular pathology often coexists with Alzheimer disease (AD) and other dementing disorders; 25-60% of dementia cases show both AD and vascular lesions. The lesion patterns in “pure” VCI with predominant multiple small (subcortical) lesions related to arteriosclerosis and microangiopathies and in mixed dementia (AD associated with vascular encephalopathy), more often showing large infarcts, suggest different pathogenesis of both types of lesions. Due to the high variability of cerebrovascular pathology and its causative factors no validated neuropathological criteria exist for VCI and mixed dementia. In very old subjects selective hippocampal sclerosis may be associated with multiple other vascular pathologies. Minor cerebrovascular lesions, except for severe amyloid angiopathy, appear not essential for cognitive decline in full-blown AD, while both mild AD-type pathology and small vessel disease may interact synergistically in “unmasking” or promoting dementia. AD pathology is significantly less severe in the presence of cerebrovascular lesions. Further studies are needed to validate diagnostic criteria for VaD/VCI and to clarify the impact of vascular lesions on cognitive impairment as a basis for more precise clinical diagnosis, early prevention and management.