Dataset Information

Pathophysiology of vascular dementia.

ABSTRACT: The concept of Vascular Dementia (VaD) has been recognized for over a century, but its definition and diagnostic criteria remain unclear. Conventional definitions identify the patients too late, miss subjects with cognitive impairment short of dementia, and emphasize consequences rather than causes, the true bases for treatment and prevention. We should throw out current diagnostic categories and describe cognitive impairment clinically and according to commonly agreed instruments that document the demographic data in a standardized manner and undertake a systematic effort to identify the underlying aetiology in each case. Increased effort should be targeted towards the concept of and criteria for Vascular Cognitive Impairment and Post-Stroke Dementia as well as for genetic factors involved, especially as these categories hold promise for early prevention and treatment.

SUBMITTER: Iemolo F

PROVIDER: S-EPMC2784430 | biostudies-literature | 2009 Nov

REPOSITORIES: biostudies-literature

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Pathophysiology of vascular dementia.

Iemolo Francesco F Duro Giovanni G Rizzo Claudia C Castiglia Laura L Hachinski Vladimir V Caruso Calogero C

Immunity & ageing : I & A 20091106

The concept of Vascular Dementia (VaD) has been recognized for over a century, but its definition and diagnostic criteria remain unclear. Conventional definitions identify the patients too late, miss subjects with cognitive impairment short of dementia, and emphasize consequences rather than causes, the true bases for treatment and prevention. We should throw out current diagnostic categories and describe cognitive impairment clinically and according to commonly agreed instruments that document ...[more]

PMID: 19895675

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Project description:Little is known about the contributors and physiological responses to white matter hypoperfusion in the human brain. We previously showed the ratio of myelin-associated glycoprotein to proteolipid protein 1 in post-mortem human brain tissue correlates with the degree of ante-mortem ischaemia. In age-matched post-mortem cohorts of Alzheimer's disease (n = 49), vascular dementia (n = 17) and control brains (n = 33) from the South West Dementia Brain Bank (Bristol), we have now examined the relationship between the ratio of myelin-associated glycoprotein to proteolipid protein 1 and several other proteins involved in regulating white matter vascularity and blood flow. Across the three cohorts, white matter perfusion, indicated by the ratio of myelin-associated glycoprotein to proteolipid protein 1, correlated positively with the concentration of the vasoconstrictor, endothelin 1 (P = 0.0005), and negatively with the concentration of the pro-angiogenic protein, vascular endothelial growth factor (P = 0.0015). The activity of angiotensin-converting enzyme, which catalyses production of the vasoconstrictor angiotensin II was not altered. In samples of frontal white matter from an independent (Oxford, UK) cohort of post-mortem brains (n = 74), we confirmed the significant correlations between the ratio of myelin-associated glycoprotein to proteolipid protein 1 and both endothelin 1 and vascular endothelial growth factor. We also assessed microvessel density in the Bristol (UK) samples, by measurement of factor VIII-related antigen, which we showed to correlate with immunohistochemical measurements of vessel density, and found factor VIII-related antigen levels to correlate with the level of vascular endothelial growth factor (P = 0.0487), suggesting that upregulation of vascular endothelial growth factor tends to increase vessel density in the white matter. We propose that downregulation of endothelin 1 and upregulation of vascular endothelial growth factor in the context of reduced ratio of myelin-associated glycoprotein to proteolipid protein 1 are likely to be protective physiological responses to reduced white matter perfusion. Further analysis of the Bristol cohort showed that endothelin 1 was reduced in the white matter in Alzheimer's disease (P < 0.05) compared with control subjects, but not in vascular dementia, in which endothelin 1 tended to be elevated, perhaps reflecting abnormal regulation of white matter perfusion in vascular dementia. Our findings demonstrate the potential of post-mortem measurement of myelin proteins and mediators of vascular function, to assess physiological and pathological processes involved in the regulation of cerebral perfusion in Alzheimer's disease and vascular dementia.

Project description:For patients with a diagnosis of vascular dementia there is evidence that aspirin is widely prescribed - in one study, completed by geriatricians and psychiatrists in the UK, 80% of patients with cognitive impairment (with vascular risk factors) were prescribed aspirin. However, a number of queries remain unanswered: Is there convincing evidence that aspirin benefits patients with vascular dementia? Does aspirin affect cognition or improve prognosis? In addition, does the risk of cerebral or gastric haemorrhage outweigh any benefit?To assess the evidence of effectiveness of the use of aspirin for vascular dementia.Computerized databases were searched independently by two reviewers. In addition, relevant websites were searched and some journals were handsearched. Specialists in the field were approached for unpublished material and any publications found were searched for additional references. The most recent search for trials was carried out in February 2000.All randomized controlled trials investigating the effect of aspirin for vascular dementia are included. Inclusion/exclusion of studies comprised systematic assessment of the quality of study design and the risk of bias.Data were extracted independently by both reviewers, using a previously tested data extraction form and, where required, authors were contacted for data not provided in the papers. The aim is to evaluate data recorded via tools assessing cognitive and behavioural changes along with mortality, morbidity and institutionalization data.No trials are eligible for inclusion in this review.There is no evidence that aspirin is effective in treating patients with a diagnosis of vascular dementia. Further research is needed to assess the effect of aspirin on cognition, and on other outcomes such as behaviour, and quality of life. At present there is no evidence relating to other queries about the use of aspirin for dementia (these are described in the Background section of this review). The most recent search for references to relevant research was carried out in February 2000, but no new evidence was found.

Dataset Information

Pathophysiology of vascular dementia.

Publications

Pathophysiology of vascular dementia.

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