Pathogenetic mechanisms in vascular dementia

Parnetti, Lucilla; Mari, Daniela; Mecocci, Patrizia; Senin, Umberto

doi:10.1007/bf02592404

Cited by 15 publications

(9 citation statements)

References 79 publications

(68 reference statements)

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“…These findings can explain the higher ratio of VaD in patients with hyperfibrinogenaemia by increasing the risk for CVD. On the other hand, hyperfibrinogenaemia has been correlated with white matter lesions (29), leukoaraiosis (30), silent infarction (31) and cerebral hypoperfusion (32,33), all of which were further related to cognitive decline and VaD (34,35). These cascade effects may put patients with hyperfibrinogenaemia at increased risk for VaD even in the absence of overt CVD.…”

Section: Discussionmentioning

confidence: 99%

Plasma fibrinogen is associated with cognitive decline and risk for dementia in patients with mild cognitive impairment

Zhang

et al. 2007

International Journal of Clinical Practice

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This study was aimed to investigate the relationship between plasma fibrinogen level and risk for cognitive decline and dementia in patients with mild cognitive impairment (MCI). Elderly patients with suspected cognitive impairment were screened and evaluated periodically. One hundred and eighty-five patients who met the criteria for MCI were enrolled. Blood coagulation functions and plasma fibrinogen levels were measured at baseline. Hyperfibrinogenaemia was defined as plasma fibrinogen > or =3.0 g/l. Global cognitive function was assessed serially with Mini-Mental State Examination (MMSE). The enrolled patients were followed for 2 years to observe if dementia was developed. There were 185 patients diagnosed as MCI, of which 17 (9.2%) deceased, 15 (8.1%) lost to follow-up, and 68 (36.8%) developed dementia during follow-up. Mean of MMSE score of the enrolled patients declined significantly during follow-up (22.0 +/- 3.0 vs. 18.1 +/- 5.8, p < 0.001). Patients with hyperfibrinogenaemia at baseline had greater MMSE decrement during follow-up than patients with normal fibrinogen level (-5.4 +/- 5.4 vs. -3.5 +/- 4.5, p < 0.05). Linear regression indicated that plasma fibrinogen level was associated with cognitive decline (R = 0.17, p < 0.05). Patients with hyperfibrinogenaemia had an increased risk for dementia and vascular dementia compared with patients with normal level of plasma fibrinogen (log rank test, p < 0.05). There was a trend that hyperfibrinogenaemia also increased risk for dementia of Alzheimer's type (p = 0.061). It can be concluded that plasma fibrinogen level may be associated with cognitive decline, and hyperfibrinogenaemia may increase risk for dementia in patients with MCI.

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Section: Discussionmentioning

confidence: 99%

Plasma fibrinogen is associated with cognitive decline and risk for dementia in patients with mild cognitive impairment

Zhang

et al. 2007

International Journal of Clinical Practice

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“…Aphasia and depression, which can both be associated with VaD, may contribute to apparently poor performances in neuropsychological tests and may lead to an incorrect diagnosis of dementia. Finally, the great heterogeneity of VaD, as documented by the number of pathogenic mechanisms known to underline VaD [27], may also lead to discrepancies between studies.…”

Section: Other Methodological Issuesmentioning

confidence: 99%

Epidemiology of Vascular Dementia

Leys¹,

Pasquier²,

Parnetti³

1998

Pathophysiol Haemos Thromb

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Although epidemiological studies are limited by diagnostic uncertainties, they suggest that stroke increases the risk of dementia. The mortality rate is higher in vascular dementia (VaD) than in Alzheimer’s disease (AD). Community-based studies have provided several consistent findings: (i) age dependence with prevalence rates doubling every 5 years, (ii) a higher frequency in men and (iii) nation-to-nation differences. The prevalence of VaD ranges from 2.2% in 70- to 79-year-old women, to 16.3% in men >80 years. One sixth of acute stroke patients have preexisting dementia. The incidence of VaD has been studied much less extensively than that of AD, and substantial variations in the incidence rates have been observed: annual incidence rates (per 100,000) range from 20 to 40 between 60 and 69 years of age and from 200 to 700 over 80. The incidence rate of VaD declined over the last 2 decades, probably as a consequence of effective stroke prevention. It is generally assumed that risk factors for VaD are those of stroke, with arterial hypertension as leading factor, followed by atherosclerotic disease, low education level, alcohol abuse and heart disease. Stroke characteristics, such as lacunar infarction and left-sided hemispheric lesions, are major determinants of VaD. The cerebrovascular lesions are likely to be the only cause of dementia in strategic infarcts, in lacunar state, in hereditary cystatin C amyloid angiopathy and in CADASIL. However, white matter changes, and associated Alzheimer pathology, which are both frequent in this age category, may also contribute to the cognitive decline.

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“…Vascular dementia is a heterogeneous syndrome caused by the occlusion of large vessels or small artery disease (Hachinski et al 1987;Parnetti et al 1994;Roman 1996;Wallin and Blennow 1993). The pathogenesis of, and relationship between, the latter small artery lesions, i.e., lacunae and white matter lesions, and progressive cognitive impairment or dementia have been much debated.…”

Section: Introductionmentioning

confidence: 99%

Blood-brain barrier disruption in the hypothalamus of young adult spontaneously hypertensive rats

Ueno

Sakamoto

Liao

et al. 2004

Histochem Cell Biol

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Vascular permeability and endothelial glycocalyx were examined in young adult spontaneously hypertensive rats (SHR), stroke-prone SHR (SHRSP), and Wistar Kyoto rats (WKY) as a control, in order to determine earlier changes in the blood-brain barrier (BBB) in the hypothalamus in chronic hypertension. These rats were injected with horseradish peroxidase (HRP) as an indicator of vascular permeability. Brain slices were developed with a chromogen and further examined with cationized ferritin, a marker for evaluating glycocalyx. Staining for HRP was seen around vessels in the hypothalamus of SHR and SHRSP, but was scarce in WKY. The reaction product of HRP appeared in the abluminal pits of endothelial cells and within the basal lamina of arterioles, showing increased vascular permeability in the hypothalamus of SHR and SHRSP, whereas there were no leaky vessels in the frontal cortex of SHR and SHRSP, or in both areas of WKY. The number of cationized ferritin particles binding to the capillary endothelial cells was decreased in the hypothalamus of SHR and SHRSP, while the number decreased in the frontal cortex of SHRSP, compared with those in WKY. Cationized ferritin binding was preserved in some leaky arterioles, while it was scarce or disappeared in other leaky vessels. These findings suggest that BBB disruption occurs in the hypothalamus of 3-month-old SHR and SHRSP, and that endothelial glycocalyx is markedly damaged there without a close relationship to the early changes in the BBB.

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Pathogenetic mechanisms in vascular dementia

Cited by 15 publications

References 79 publications

Plasma fibrinogen is associated with cognitive decline and risk for dementia in patients with mild cognitive impairment

Plasma fibrinogen is associated with cognitive decline and risk for dementia in patients with mild cognitive impairment

Epidemiology of Vascular Dementia

Blood-brain barrier disruption in the hypothalamus of young adult spontaneously hypertensive rats

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