White matter changes in dementia of Alzheimer's type: the difference in vulnerability between cell compartments

Englund, Elisabet; Brun, Arne

doi:10.1111/j.1365-2559.1990.tb01542.x

Cited by 130 publications

(56 citation statements)

References 14 publications

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“…Lacunar infarcts were defined as small cystic lesions in the basal ganglia, thalamus, centrum semiovale and pons, due to lipohyalinosis [19]. The degree of WMCs was mainly evaluated on the LFB staining [20].…”

Section: Cerebrovascular Lesionsmentioning

confidence: 99%

Prevalence of small cerebral bleeds in patients with a neurodegenerative dementia: A neuropathological study

Reuck

Deramecourt

Cordonnier

et al. 2011

Journal of the Neurological Sciences

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Section: Cerebrovascular Lesionsmentioning

confidence: 99%

Prevalence of small cerebral bleeds in patients with a neurodegenerative dementia: A neuropathological study

Reuck

Deramecourt

Cordonnier

et al. 2011

Journal of the Neurological Sciences

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“…The WM lesions were graded as normal (grade 0), low (grade I; reduced meshwork density with scattered, irregularly widened axons), moderate (grade II; further reduction in meshwork density compared with grade I, mainly composed of relatively short axons), and high (grade III; depletion of axon meshwork with a few remaining long axons) according to the modified criteria proposed by Englund and Brun. 8 The areas examined in this study are schematically presented in Figure 1, and the clinicopathological profiles from all cases are summarized in Table 1. All procedures followed were in accordance with institutional guidelines, and informed consent was obtained from relatives of all subjects.…”

Section: Tissue Preparationmentioning

confidence: 99%

Upregulated Expression of 14-3-3 Proteins in Astrocytes From Human Cerebrovascular Ischemic Lesions

Kawamoto

Akiguchi

Tomimoto

et al. 2006

Stroke

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Background and Purpose-Several types of chaperone proteins, such as heat shock proteins, have been reported to be associated with brain ischemia. The purpose of this study was to investigate whether an abnormal expression of 14-3-3 proteins, a novel type of molecular chaperones, occurs in human gray and white matter ischemic lesions. Methods-We prepared formalin-fixed, paraffin-embedded sections from 33 autopsied brains, consisting of 7 normal controls, 4 cases with cerebral thrombosis, 5 cases with cerebral embolism, 8 cases with multiple lacunar infarctions, and 9 cases with Binswanger disease. Deparaffinized sections from all cases were immunostained with anti-14-3-3 antibodies using the avidin-biotin-peroxidase complex method, and some sections were also double-immunostained for 14-3-3 and glial markers. Results-In the normal control brains, 14-3-3 immunoreactivity was mainly localized to the neuronal somata and processes. Strongly 14-3-3-immunopositive astrocytes were distributed in the infarct lesions and were particularly abundant in infarcts at the chronic stage. Intensely 14-3-3-immunolabeled astrocytes were also observed in the ischemic white matter lesions, and in the severely affected white matter lesions from patients with Binswanger disease, dense 14-3-3 immunoreactivity was found in clasmatodendritic astroglia as well as in reactive astrocytes. Conclusions-Our results suggest that 14-3-3 proteins may be induced mainly in astrocytes from human cerebrovascular ischemic lesions, and that the upregulated expression of 14-3-3 proteins in astrocytes may be involved in the formation of astrogliosis.

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“…However, since the eighties, postmortem [10,11,12] and MRI studies [13,14] in AD patients provided evidence of white matter (WM) abnormalities that more recently have also been related to cognitive deficits [15,16]. …”

Section: Introductionmentioning

confidence: 99%

Insights into White Matter Damage in Alzheimer's Disease: From Postmortem to in vivo Diffusion Tensor MRI Studies

Caso¹,

Filippi²

2015

Neurodegener Dis

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Background: Alzheimer's disease (AD) has traditionally been considered a disease of the gray matter (GM). However, several pathological and neuroimaging studies provided evidence of white matter (WM) abnormalities in this disease. The advent of diffusion tensor (DT) MRI allowed researchers to study in vivo cerebral WM abnormalities in AD, including the earliest stage of the disease and its atypical variants. Objective: To provide a concise overview of the main neuropathological and DT MRI studies that explored WM damage in AD providing new insights into the underlying pathophysiological mechanisms. Results: Neuropathological studies revealed that GM and WM changes did not concur regionally in many areas, where well-preserved GM often lay over severely changed WM also in nondemented subjects with an underlying AD pathology. DT MRI studies confirmed in vivo a severe WM involvement in classical and atypical AD variants and in the prodromal stage of the disease. Microstructural WM damage was severer and more distributed than expected on the basis of cortical atrophy in all clinical AD phenotypes. Conclusions: AD is characterized by a relevant involvement of the WM as demonstrated by postmortem and in vivo evidence. WM microstructural damage in AD is not always secondary to neuronal loss, suggesting a role of other pathological mechanisms such as prion-like propagation of altered proteins or neuroinflammation. DT MRI offers new insight into AD pathophysiology and, more importantly, new possible targets for future experimental therapies.

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White matter changes in dementia of Alzheimer's type: the difference in vulnerability between cell compartments

Cited by 130 publications

References 14 publications

Prevalence of small cerebral bleeds in patients with a neurodegenerative dementia: A neuropathological study

Prevalence of small cerebral bleeds in patients with a neurodegenerative dementia: A neuropathological study

Upregulated Expression of 14-3-3 Proteins in Astrocytes From Human Cerebrovascular Ischemic Lesions

Insights into White Matter Damage in Alzheimer's Disease: From Postmortem to in vivo Diffusion Tensor MRI Studies

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