The topography of cortical microbleeds in frontotemporal lobar degeneration: a post-mortem 7.0-tesla magnetic resonance study

J, De Reuck; Auger, F.; Durieux, Nicolas; Deramecourt, Vincent; Ca, Maurage; Lebert, Florence; Leys, Didier; Cordonnier, Charlotte; Pasquier, Florence; Bordet, Régis

doi:10.5114/fn.2016.60364

Cited by 6 publications

(6 citation statements)

References 22 publications

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“…21,22 Also the presence of cortical microbleeds are linked to the degenerative process (23). However, some recent MRI studies show that WMCs are more distributed than the grey matter lesions, suggesting two separate types of neurodegenerative pathology in FTLD.…”

Section: Discussionmentioning

confidence: 99%

Topographic distribution of white matter changes and lacunar infarcts in neurodegenerative and vascular dementia syndromes: A post-mortem 7.0-tesla magnetic resonance imaging study

Reuck

Auger

Durieux

et al. 2016

European Stroke Journal

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Background: White matter changes and lacunar infarcts are regarded as linked to the same underlying small-vessel pathology. On magnetic resonance imaging, white matter changes are frequently observed, while the number of lacunar infarcts is probably underestimated. The present study post-mortem 7.0-tesla magnetic resonance imaging study compares the severity and the distribution of white matter changes and lacunar infarcts in different neurodegenerative and vascular dementia syndromes in order to determine their impact on the disease evolution. Patients and methods: Eighty-four post-mortem brains consisting of 15 patients with pure Alzheimer's disease and 12 with associated cerebral amyloid angiopathy, 14 patients with frontotemporal lobar degeneration, 7 with Lewy body dementia, 10 with progressive supranuclear palsy, 14 with vascular dementia and 12 control brains were examined. Six hemispheric coronal sections of each brain underwent 7.0-tesla magnetic resonance imaging. Location and severity of white matter changes and lacunar infarcts were evaluated semi-quantitatively in each section separately. Results: White matter changes predominated in the prefrontal and frontal sections of frontotemporal lobar degeneration and in the post-central section of associated cerebral amyloid angiopathy brains, while overall increased in vascular dementia cases. Lacunar infarcts were more frequent in the vascular dementia brains and mainly increased in the centrum semiovale. Conclusions: White matter changes have a different topographic distribution in neurodegenerative diseases and are most severe and extended in vascular dementia. Lacunar infarcts predominate in the deep white matter of vascular dementia compared to the neurodegenerative diseases. Vascular cognitive impairment is mainly linked to white matter changes due to chronic ischaemia as well as to lacunar infarcts due to small-vessel occlusion.

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Section: Discussionmentioning

confidence: 99%

Topographic distribution of white matter changes and lacunar infarcts in neurodegenerative and vascular dementia syndromes: A post-mortem 7.0-tesla magnetic resonance imaging study

Reuck

Auger

Durieux

et al. 2016

European Stroke Journal

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“…Microbleeds are currently not known to be causative or reactionary to the conditions of ALS. Studies have linked cortical microbleeds (CMBs) with Alzheimer's disease [92, 93] and shown that CMBs, while rare in frontotemporal lobar degeneration, are increased in the regions affected by neurodegenerative lesions. This suggests that the progression of Alzheimer's disease promotes CMBs.…”

Section: Microbleedsmentioning

confidence: 99%

Pathomechanisms of Blood-Brain Barrier Disruption in ALS

Kakaroubas

Brennan²,

Keon³

et al. 2019

Neuroscience Journal

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The blood-brain barrier (BBB) and the blood-spinal cord barrier (BSCB) are responsible for controlling the microenvironment within neural tissues in humans. These barriers are fundamental to all neurological processes as they provide the extreme nutritional demands of neural tissue, remove wastes, and maintain immune privileged status. Being a semipermeable membrane, both the BBB and BSCB allow the diffusion of certain molecules, whilst restricting others. In amyotrophic lateral sclerosis (ALS) and other neurodegenerative diseases, these barriers become hyperpermeable, allowing a wider variety of molecules to pass through leading to more severe and more rapidly progressing disease. The intention of this review is to discuss evidence that BBB hyperpermeability is potentially a disease driving feature in ALS and other neurodegenerative diseases. The various biochemical, physiological, and genomic factors that can influence BBB permeability in ALS and other neurodegenerative diseases are also discussed, in addition to novel therapeutic strategies centred upon the BBB.

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“…Relationships between CMBs and other neurodegenerative and neuroinflammatory pathologies have also been hypothesized, 10,38 although they have not been directly confirmed in neuropathology. Therefore, it cannot be excluded that the investigation of further pathological hallmarks could inform us on the genesis of these lesions.…”

Section: Discussionmentioning

confidence: 99%

Histopathological Correlates of Lobar Microbleeds in False‐Positive Cerebral Amyloid Angiopathy Cases

Perosa,

Auger,

Zanon Zotin

et al. 2023

Annals of Neurology

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ObjectiveA definite diagnosis of cerebral amyloid angiopathy (CAA), characterized by the accumulation of Amyloid‐β in walls of cerebral small vessels, can only be obtained through pathological examination. A diagnosis of probable CAA during life relies on the presence of haemorrhagic markers, including lobar cerebral microbleeds (CMBs). The aim of this project was to study the histopathological correlates of lobar CMBs in false‐positive CAA cases.MethodsIn three patients who met criteria for probable CAA during life, but showed no CAA upon neuropathological examination, lobar CMBs were counted on ex vivo 3 T MRI and on ex vivo 7 T MRI. Areas with lobar CMBs were next sampled and cut in serial sections, on which the CMBs were then identified.ResultsCollectively, there were 25 lobar CMBs on in vivo MRI and 22 on ex vivo 3 T MRI of the analysed hemispheres. On ex vivo MRI we targeted 12 CMBs for sampling and definite histopathological correlates were retrieved for 9 of them of which seven were true CMBs. No CAA was found on any of the serial sections. The ‘culprit vessels’ associated with the true CMBs instead showed moderate to severe arteriolosclerosis. Furthermore, CMBs in false‐positive CAA cases tended to be located more often in the juxtacortical or subcortical white matter, than in the cortical ribbon.InterpretationThese findings suggest that arteriolosclerosis can generate lobar CMBs and that more detailed investigations into the exact localization of CMBs with respect to the cortical ribbon could potentially aid the diagnosis of CAA during life.This article is protected by copyright. All rights reserved.

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The topography of cortical microbleeds in frontotemporal lobar degeneration: a post-mortem 7.0-tesla magnetic resonance study

Cited by 6 publications

References 22 publications

Topographic distribution of white matter changes and lacunar infarcts in neurodegenerative and vascular dementia syndromes: A post-mortem 7.0-tesla magnetic resonance imaging study

Topographic distribution of white matter changes and lacunar infarcts in neurodegenerative and vascular dementia syndromes: A post-mortem 7.0-tesla magnetic resonance imaging study

Pathomechanisms of Blood-Brain Barrier Disruption in ALS

Histopathological Correlates of Lobar Microbleeds in False‐Positive Cerebral Amyloid Angiopathy Cases

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