Alzheimer Disease: Bogousslavsky J

Assal F, Sztajzel R, Carota A, Annoni JM, Bogousslavsky J. · Clinique de neurologie HUG, 1211 Gennève. · Rev Med Suisse. · Pubmed #16734190 No free full text.

Abstract: Neurodegenerative and cerebrovascular diseases have been related for more than a century. Epidemiological data show that main vascular risk factors are also risk factors for Alzheimer disease. Experimental evidences demonstrate that some of those risk factors accelerate the progress of Alzheimer lesions, mainly by acting on the amyloid cascade. Recent advances in understanding the basic mechanisms of CADASIL and familial amyloid angiopathy reveal that these forms of vascular dementias are degenerative disease of brain vessels. Modern neuroimaging techniques will allow to better understand relations between symptomatic strokes, silent infarcts, leukoaraiosis, microbleeds and degenerative pathology before the stage of dementia.

Leys D, Erkinjuntti T, Desmond DW, Schmidt R, Englund E, Pasquier F, Parnetti L, Ghika J, Kalaria RN, Chabriat H, Scheltens P, Bogousslavsky J. · University of Lille, France. · Alzheimer Dis Assoc Disord. · Pubmed #10609680 No free full text.

Abstract: Although vascular dementia (VaD) is the second most frequent cause of dementia after Alzheimer disease (AD), the concept remains controversial in terms of delineation. The objective of this review is to investigate, from available literature, the role of cerebral infarcts in the pathogenesis of VaD and to identify areas of interest that need further evaluation and research. The incidence of new onset dementia is increased after stroke. Stroke subtypes, total volume of cerebral infarction and functional tissue loss, and location of the lesions are probably the major determinants of VaD. Any cause of stroke can lead to VaD. In some circumstances the causal relation between stroke and dementia is clear: (1) in young patients who are unlikely to have associated Alzheimer pathology; (2) when the cognitive functioning was normal before stroke, impaired immediately after, and does not worsen over time; (3) when the lesions are located in strategic areas; and (4) when a well-defined vasculopathy known to cause dementia is proven. However, several issues remain unsolved in VaD: lack of specificity of the diagnostic criteria; influence of white matter changes and associated Alzheimer pathology; influence of preexisting cognitive status; possibility of having VaD without stroke and the clinical relevance of silent infarcts to VaD; and best therapeutic strategy to be used to prevent VaD and to prevent stroke in patients with VaD. These questions form the basis for proposals for future research.