Scientific correspondence

Larionov, Sergey; Dedeck, Oliver; Birkenmeier, Gerd; Orantes, M; Ghebremedhin, Estifanos; Thal, Dietmar Rudolf

doi:10.1111/j.1365-2990.2006.00743.x

Cited by 8 publications

(9 citation statements)

References 22 publications

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“…This observation is based on the data obtained from 82 non-selected autopsy cases. The circle of Willis was observed macroscopically for the presence or absence of the 11 arteries of the circle of Willis as previously described [70]. The extent of AS was calculated as: number of AS-affected vessels × 100/number of investigated vessels of the circle of Willis [70].…”

Section: Pathology Of Major Vessel Disorders In the Aging Brainmentioning

confidence: 99%

“…The circle of Willis was observed macroscopically for the presence or absence of the 11 arteries of the circle of Willis as previously described [70]. The extent of AS was calculated as: number of AS-affected vessels × 100/number of investigated vessels of the circle of Willis [70]. The cases analyzed here were already included in other studies under other aspects [65, 70]…”

Section: Pathology Of Major Vessel Disorders In the Aging Brainmentioning

confidence: 99%

“…The extent of AS was calculated as: number of AS-affected vessels × 100/number of investigated vessels of the circle of Willis [70]. The cases analyzed here were already included in other studies under other aspects [65, 70]…”

Section: Pathology Of Major Vessel Disorders In the Aging Brainmentioning

confidence: 99%

“…α2-macroglobulin (A2M; Fig. 1), neutrophil elastase] in the AS plaque [70, 117]. Arterial hypertension is a well-known risk factor for AS [76] and may foster plasma protein leakage into the vessel wall.…”

Section: Pathology Of Major Vessel Disorders In the Aging Brainmentioning

confidence: 99%

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Vascular pathology in the aged human brain

2010

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Cerebral atherosclerosis (AS), small vessel disease (SVD), and cerebral amyloid angiopathy (CAA) are the most prevalent arterial disorders in the aged brain. Pathogenetically, AS and SVD share similar mechanisms: plasma protein leakage into the vessel wall, accumulation of lipid-containing macrophages, and fibrosis of the vessel wall. CAA, on the other hand, is characterized by the deposition of the amyloid β-protein in the vessel wall. Despite these differences between CAA, AS and SVD, apolipoprotein E (apoE) is involved in all three disorders. Such a pathogenetic link may explain the correlations between AS, SVD, CAA, and Alzheimer’s disease in the brains of elderly individuals reported in the literature. In addition, AS, SVD, and CAA can lead to tissue lesions such as hemorrhage and infarction. Moreover, intracerebral SVD leads to plasma protein leakage into the damaged vessel wall and into the perivascular space resulting in a blood–brain barrier (BBB) dysfunction. This SVD-related BBB dysfunction is considered to cause white matter lesions (WMLs) and lacunar infarcts. In this review, we demonstrate the relationship between AS, SVD, and CAA as well as their contribution to the development of vascular tissue lesions and we emphasize an important role for apoE in the pathogenesis of vessel disorders and vascular tissue lesions as well as for BBB dysfunction on WML and lacunar infarct development.

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Section: Pathology Of Major Vessel Disorders In the Aging Brainmentioning

confidence: 99%

Section: Pathology Of Major Vessel Disorders In the Aging Brainmentioning

confidence: 99%

Section: Pathology Of Major Vessel Disorders In the Aging Brainmentioning

confidence: 99%

Section: Pathology Of Major Vessel Disorders In the Aging Brainmentioning

confidence: 99%

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Vascular pathology in the aged human brain

2010

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“… Determinations: AS severity (Larionov et al, 2006): 0 = no AS, 1 = no more than three AS-plaques in an artery and no circular AS-plaques, 2 = more than three plaques in at least one artery but no concentric plaques, 3 = more than three plaques in at least one vessel and concentric plaques; SVD severity (Kolsch et al, 2007): 0 = no SVD, 1 = single (1–3) vessels exhibit SVD in one area of the brain, 2 = more than 3 vessels in at least one brain area exhibit SVD, 3 = in more than two brain regions more than 3 vessels are affected by SVD; CAA severity (Vonsattel et al, 1991): 0 = no CAA, 1 = Aβ deposits in the vessel wall without loss of smooth muscle cells in the vessel wall, 2 = Aβ deposits in the vessel wall accompanied by degeneration of the smooth muscle cell layer, 3 = extensive Aβ deposition and focal vessel wall fragmentations, microaneurysms, signs of hemorrhage, and fibrinoid necrosis. Abbreviations: Aβ = amyloid β-protein, AS = Atherosclerosis, CAA = cerebral amyloid angiopathy, n = number of cases studied, p = p-value assessed by partial correlation analysis controlled for gender, r = correlation coefficient assessed by partial correlation analysis controlled for gender, SVD = small vessel disease, VaD = vascular dementia. …”

Section: Figmentioning

confidence: 99%

Vascular dementia: Different forms of vessel disorders contribute to the development of dementia in the elderly brain

Thal

Grinberg

Attems

2012

Experimental Gerontology

183

141

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The diagnosis of vascular dementia (VaD) describes a group of various vessel disorders with different types of vascular lesions that finally contribute to the development of dementia. Most common forms of VaD in the elderly brain are subcortical vascular encephalopathy, strategic infarct dementia, and the multi infarct encephalopathy. Hereditary forms of VaD are rare. Most common is the cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). Sporadic forms of VaD are caused by degenerative vessel disorders such as atherosclerosis, small vessel disease (SVD) including small vessel arteriosclerosis, arteriolosclerosis, and lipohyalinosis, and cerebral amyloid angiopathy (CAA). Less frequently inflammatory vessel disorders and tumor-associated vessel lesions (e.g. angiocentric T-cell or angiotropic large cell lymphoma) can cause symptoms of dementia. Here, we review and discuss the impact of vessel disorders to distinct vascular brain tissue lesions and to the development of dementia in elderly individuals. The impact of coexisting neurodegenerative pathology in the elderly brain to VaD as well as the correlation between SVD and CAA expansion in the brain parenchyma with that of Alzheimer’s disease (AD)-related pathology is highlighted. We conclude that “pure” VaD is rare and most frequently caused by infarctions. However, there is a significant contribution of vascular lesions and vessel pathology to the development of dementia that may go beyond tissue damage due to vascular lesions. Insufficient blood blow and alterations of the perivascular drainage mechanisms of the brain may also lead to a reduced protein clearance from extracellular space and subsequent increase of proteins in the brain parenchyma, such as the amyloid β-protein, and foster, thereby, the development of AD-related neurodegeneration. As such, it seems to be important for clinical practice to consider treatment of potentially coexisting AD pathology in cognitively impaired patients with vascular lesions.

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Expression of α2-macroglobulin, neutrophil elastase, and interleukin-1α differs in early-stage and late-stage atherosclerotic lesions in the arteries of the circle of Willis

et al. 2006

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Different types of atherosclerotic (AS) lesions can be distinguished histologically and represent different stages of AS plaque development. Late-stage lesions more frequently develop complications such as plaque rupture and thrombosis with vessel occlusion than early AS lesions. To clarify whether protective, destructive, and inflammatory proteins are differentially expressed in early-stage and late-stage AS plaques we examined the proteinase inhibitor alpha(2)-macroglobulin (A2M), the neutrophil elastase (NE)-an enzyme degrading elastin and collagen fibers-and the proinflammatory protein interleukin-1alpha (IL-1alpha) in all types of AS plaques in the arteries of the circle of Willis from 78 human autopsy cases of both genders (61-91 years of age). Paraffin sections of AS plaques were immunostained with antibodies directed against A2M, NE and IL-1alpha. In initial AS lesions A2M was found, whereas NE and IL-1alpha were absent. NE and IL-1alpha became detectable as soon as a significant number of macrophages occurred within AS lesions. With increasing histopathological type of AS lesions, a marked increase of the area of the plaque exhibiting NE and IL-1alpha was observed. The area which exhibits A2M in AS plaques, on the other hand, did not vary significantly between the different stages. Thus, our results indicate a disproportionately high increase of the destructive enzyme NE and the proinflammatory protein IL-1alpha in relation to A2M with the progression of the grade of AS lesions pointing to the transgression of the protective capacity of A2M by NE and IL-1alpha in late-stage plaques. Therefore, our findings support the hypothesis that NE-induced tissue damage in late-stage AS plaques contributes to the development of plaque rupture and subsequent thrombosis.

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Scientific correspondence

Cited by 8 publications

References 22 publications

Vascular pathology in the aged human brain

Vascular pathology in the aged human brain

Vascular dementia: Different forms of vessel disorders contribute to the development of dementia in the elderly brain

Expression of α2-macroglobulin, neutrophil elastase, and interleukin-1α differs in early-stage and late-stage atherosclerotic lesions in the arteries of the circle of Willis

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