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Article ; Online: Acute Microbleeds and Microinfarcts Within the Perihematomal Area After Intracerebral Hemorrhage.

Puy, Laurent / Rauch, Antoine / Deramecourt, Vincent / Cordonnier, Charlotte / Bérézowski, Vincent

2023 Volume 54, Issue 3, Page(s) e58–e62

Abstract: Background: To further our understanding of the pathophysiology of spontaneous intracerebral hemorrhage (ICH) and related injury, we provided a postmortem neuropathological examination of acute microvascular lesions (microbleeds and microinfarcts) ... ...

Abstract	Background: To further our understanding of the pathophysiology of spontaneous intracerebral hemorrhage (ICH) and related injury, we provided a postmortem neuropathological examination of acute microvascular lesions (microbleeds and microinfarcts) within the perihematomal area. Methods: We included all consecutive cases (2005-2019) from the Lille University Hospital brain bank of ICH patients who died within the first month. Paraffin-embedded tissue sections from the perihematomal area were processed for several stainings and immunolabelings to investigate the presence of acute microbleeds and microinfarcts in the perihematomal area and to characterize surrounding neuronal and systemic inflammatory reaction (macrophages and neutrophils). Results: We included 14 ICH cases (median age, 78 years; 10 females). Acute microbleeds were observed in the perihematomal area in 12/14 patients (86%, ranging from 1 through >10) and microinfarcts in 5/14 (36%, ranging from 1 through 4). Microbleeds were observed whatever the delay from ICH onset to death was, while most cases with acute microinfarcts were observed between day 3 and day 7 (n=3/5). Both lesions were characterized by an abundant accumulation of systemic inflammatory cells and necrotic areas. Conclusions: Acute microbleeds and microinfarcts might contribute to the propagation of secondary brain tissue damages after ICH. Our examinations also question the potential role of massive systemic inflammatory cells recruitment in the genesis of these microvascular injuries.
MeSH term(s)	Female ; Humans ; Aged ; Cerebral Hemorrhage/complications ; Cerebral Hemorrhage/pathology ; Brain/pathology ; Brain Edema/pathology
Language	English
Publishing date	2023-02-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80381-9
ISSN	1524-4628 ; 0039-2499 ; 0749-7954
ISSN (online)	1524-4628
ISSN	0039-2499 ; 0749-7954
DOI	10.1161/STROKEAHA.122.040908
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Zs.A 448: Show issues

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Article ; Online: Brain Peri-Hematomal Area, a Strategic Interface for Blood Clearance: A Human Neuropathological and Transcriptomic Study.

Puy, Laurent / Perbet, Romain / Figeac, Martin / Duchêne, Bélinda / Deramecourt, Vincent / Cordonnier, Charlotte / Bérézowski, Vincent

Stroke

2022 Volume 53, Issue 6, Page(s) 2026–2035

Abstract: Background: Enhancing the blood clearance process is a promising therapeutic strategy for intracerebral hemorrhage (ICH). We aimed to investigate the kinetic of this process after ICH in human brain tissue through the monocyte-macrophage scavenger ... ...

Abstract	Background: Enhancing the blood clearance process is a promising therapeutic strategy for intracerebral hemorrhage (ICH). We aimed to investigate the kinetic of this process after ICH in human brain tissue through the monocyte-macrophage scavenger receptor (CD163)/HO-1 (hemoxygenase-1) pathway. Methods: We led a cross-sectional post-mortem study including 22 consecutive ICH cases (2005-2019) from the Lille Neurobank. Cases were grouped according to the time of death: ≤72 hours, 4 to 7 days, 8 to 15 days, 16 to 90 days, and >90 days after ICH onset. Paraffin-embedded tissue was extracted from 4 strategic areas, including hematoma core and peri-hematomal area to perform histological investigations. Additionally, we extracted RNA from the peri-hematomal area of 6 cases to perform transcriptomic analysis. Results: We included 19 ICH cases (median age: 79 [71-89] years; median delay ICH-death: 13 [5-41] days). The peri-hematomal area concentrated most of reactive microglia, CD163/HO-1 and iron deposits as compared with other brain areas. We found a surge in the blood clearance process from day 8 to day 15 after ICH onset. Transcriptomic analysis showed that HO-1 was the most upregulated gene (2.81±0.39, adjusted Conclusions: We provide histological and transcriptomic-based evidence in humans for the key role of peri-hematomal area in endogenous blood clearance process through the CD163/HO-1 pathway, especially from day 8 after ICH and favored by an anti-inflammatory environment. Our findings contribute to identify innovative therapeutic strategies for ICH.
MeSH term(s)	Aged ; Brain/pathology ; Cerebral Hemorrhage/drug therapy ; Cross-Sectional Studies ; Hematoma/drug therapy ; Humans ; Transcriptome
Language	English
Publishing date	2022-04-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80381-9
ISSN	1524-4628 ; 0039-2499 ; 0749-7954
ISSN (online)	1524-4628
ISSN	0039-2499 ; 0749-7954
DOI	10.1161/STROKEAHA.121.037751
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Article ; Online: Neutrophil extracellular traps (NETs) infiltrate haematoma and surrounding brain tissue after intracerebral haemorrhage: A post-mortem study.

Puy, Laurent / Corseaux, Delphine / Perbet, Romain / Deramecourt, Vincent / Cordonnier, Charlotte / Bérézowski, Vincent

Neuropathology and applied neurobiology

2021 Volume 47, Issue 6, Page(s) 867–877

Abstract: Aims: Because of their prothrombotic and neuroinflammatory effects, neutrophils and neutrophil extracellular traps (NETs) represent interesting therapeutic targets for spontaneous intracerebral haemorrhage (sICH). We investigated the presence, spatial ... ...

Abstract	Aims: Because of their prothrombotic and neuroinflammatory effects, neutrophils and neutrophil extracellular traps (NETs) represent interesting therapeutic targets for spontaneous intracerebral haemorrhage (sICH). We investigated the presence, spatial and temporal distribution of NETs in a human sICH post-mortem study. Methods: From 2005 to 2019, all sICH patients who came to autopsy within the first month after stroke were included and grouped according to the timing of death: 72 h, 4-7 days, 8-15 days and >15 days after ICH onset. Paraffin-embedded tissue was extracted from four strategic areas: haematoma, peri-haematomal area, ipsilateral surrounding brain tissue and a control contralateral area. Myeloperoxidase and histone H3 citrulline were immunolabelled to detect neutrophils and NETs respectively. Results: Neutrophils were present in the brains of the 14 cases (4 men, median age: 78 years) and NETs were found in 7/14 cases. Both neutrophils and NETs were detected within the haematoma but also in the surrounding tissue. The appearance of neutrophils and NETs was time-dependent, following a two-wave pattern: during the first 72 h and between 8 and 15 days after ICH onset. Qualitative examination showed that neutrophils and NETs were mainly located around dense fibrin fibres within the haematoma. Conclusions: These observations provide evidence for NETs infiltration in the brain of patients who die from sICH. NETs might interact with early haemostasis within the haematoma core, and with the surrounding neuroinflammatory response. These findings open research perspectives for NETs in the treatment of sICH injuries.
MeSH term(s)	Brain/metabolism ; Brain/pathology ; Cerebral Hemorrhage/metabolism ; Cerebral Hemorrhage/pathology ; Extracellular Traps/metabolism ; Hematoma/metabolism ; Hematoma/pathology ; Humans ; Neutrophils/metabolism ; Neutrophils/pathology ; Peroxidase/metabolism ; Stroke/metabolism ; Stroke/pathology
Chemical Substances	Peroxidase (EC 1.11.1.7)
Language	English
Publishing date	2021-06-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80371-6
ISSN	1365-2990 ; 0305-1846
ISSN (online)	1365-2990
ISSN	0305-1846
DOI	10.1111/nan.12733
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Article ; Online: Neuronal substrate of cognitive impairment in post-stroke dementia.

Deramecourt, Vincent / Pasquier, Florence

Brain : a journal of neurology

2014 Volume 137, Issue Pt 9, Page(s) 2404–2405

MeSH term(s)	Aging/pathology ; Dementia, Vascular/diagnosis ; Female ; Humans ; Male ; Prefrontal Cortex/pathology ; Pyramidal Cells/pathology
Language	English
Publishing date	2014-09
Publishing country	England
Document type	Comment ; Journal Article
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awu188
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Article ; Online: Tau Transfer via Extracellular Vesicles Disturbs the Astrocytic Mitochondrial System.

Perbet, Romain / Zufferey, Valentin / Leroux, Elodie / Parietti, Enea / Espourteille, Jeanne / Culebras, Lucas / Perriot, Sylvain / Du Pasquier, Renaud / Bégard, Séverine / Deramecourt, Vincent / Déglon, Nicole / Toni, Nicolas / Buée, Luc / Colin, Morvane / Richetin, Kevin

Cells

2023 Volume 12, Issue 7

Abstract: Tauopathies are neurodegenerative disorders involving the accumulation of tau isoforms in cell subpopulations such as astrocytes. The origins of the 3R and 4R isoforms of tau that accumulate in astrocytes remain unclear. Extracellular vesicles (EVs) were ...

Abstract	Tauopathies are neurodegenerative disorders involving the accumulation of tau isoforms in cell subpopulations such as astrocytes. The origins of the 3R and 4R isoforms of tau that accumulate in astrocytes remain unclear. Extracellular vesicles (EVs) were isolated from primary neurons overexpressing 1N3R or 1N4R tau or from human brain extracts (progressive supranuclear palsy or Pick disease patients or controls) and characterized (electron microscopy, nanoparticle tracking analysis (NTA), proteomics). After the isolated EVs were added to primary astrocytes or human iPSC-derived astrocytes, tau transfer and mitochondrial system function were evaluated (ELISA, immunofluorescence, MitoTracker staining). We demonstrated that neurons in which 3R or 4R tau accumulated had the capacity to transfer tau to astrocytes and that EVs were essential for the propagation of both isoforms of tau. Treatment with tau-containing EVs disrupted the astrocytic mitochondrial system, altering mitochondrial morphology, dynamics, and redox state. Although similar levels of 3R and 4R tau were transferred, 3R tau-containing EVs were significantly more damaging to astrocytes than 4R tau-containing EVs. Moreover, EVs isolated from the brain fluid of patients with different tauopathies affected mitochondrial function in astrocytes derived from human iPSCs. Our data indicate that tau pathology spreads to surrounding astrocytes via EVs-mediated transfer and modifies their function.
MeSH term(s)	Humans ; tau Proteins/metabolism ; Astrocytes/metabolism ; Tauopathies/pathology ; Brain/metabolism ; Protein Isoforms/metabolism
Chemical Substances	tau Proteins ; Protein Isoforms
Language	English
Publishing date	2023-03-23
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12070985
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Article: Neuropathology of frontotemporal lobar degeneration: a review.

Bahia, Valéria Santoro / Takada, Leonel Tadao / Deramecourt, Vincent

Dementia & neuropsychologia

2017 Volume 7, Issue 1, Page(s) 19–26

Abstract: Frontotemporal lobar degeneration (FTLD) is the second most common cause of presenile dementia. Three main clinical variants are widely recognized within the FTLD spectrum: the behavioural variant of frontotemporal dementia (bvFTD), semantic dementia (SD) ...

Abstract	Frontotemporal lobar degeneration (FTLD) is the second most common cause of presenile dementia. Three main clinical variants are widely recognized within the FTLD spectrum: the behavioural variant of frontotemporal dementia (bvFTD), semantic dementia (SD) and progressive non-fluent aphasia (PNFA). FTLD represents a highly heterogeneous group of neurodegenerative disorders which are best classified according to the main protein component of pathological neuronal and glial inclusions. The most common pathological class of FTLD is associated with the TDP-43 protein (FTLD-TDP), while FTLD-Tau is considered slightly less common while the FTLD-FUS (Fused in sarcoma protein) pathology is rare. In this review, these three major pathological types of FTLD are discussed.
Language	English
Publishing date	2017-11-30
Publishing country	Brazil
Document type	Journal Article ; Review
ISSN	1980-5764
ISSN	1980-5764
DOI	10.1590/S1980-57642013DN70100004
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Article ; Online: Association of Amyotrophic Lateral Sclerosis and Alzheimer's Disease: New Entity or Coincidence? A Case Series.

Vrillon, Agathe / Deramecourt, Vincent / Pasquier, Florence / Magnin, Éloi / Wallon, David / Lozeron, Pierre / Bouaziz-Amar, Élodie / Paquet, Claire

Journal of Alzheimer's disease : JAD

2021 Volume 84, Issue 4, Page(s) 1439–1446

Abstract: Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia have a strong clinical, genetic, and pathological connection but association of ALS with Alzheimer's disease (AD) is seldom reported. We report a series of 5 cases of AD associated with ALS. ...

Abstract	Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia have a strong clinical, genetic, and pathological connection but association of ALS with Alzheimer's disease (AD) is seldom reported. We report a series of 5 cases of AD associated with ALS. Our patients presented with cognitive deterioration with episodic memory impairment meeting criteria for AD. ALS occurred subsequently in all cases and its phenotype was not homogenous. Amyloid process was confirmed in four cases with cerebrospinal fluid biomarkers. One case underwent postmortem exam, demonstrating hallmarks lesions of both diseases. This series highlights that ALS-AD phenotype could be a specific underexplored entity.
MeSH term(s)	Aged ; Aged, 80 and over ; Alzheimer Disease/pathology ; Amyloid/cerebrospinal fluid ; Amyotrophic Lateral Sclerosis/pathology ; Biomarkers/cerebrospinal fluid ; Brain/pathology ; Cognition Disorders/pathology ; Female ; Humans ; Male ; Memory Disorders/pathology ; Neuropsychological Tests/statistics & numerical data
Chemical Substances	Amyloid ; Biomarkers
Language	English
Publishing date	2021-10-07
Publishing country	Netherlands
Document type	Case Reports ; Letter
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-215226
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Article ; Online: The TMEM240 Protein, Mutated in SCA21, Is Expressed in Purkinje Cells and Synaptic Terminals.

Homa, Mégane / Loyens, Anne / Eddarkaoui, Sabiha / Faivre, Emilie / Deramecourt, Vincent / Maurage, Claude-Alain / Buée, Luc / Huin, Vincent / Sablonnière, Bernard

Cerebellum (London, England)

2020 Volume 19, Issue 3, Page(s) 358–369

Abstract: A variety of missense mutations and a stop mutation in the gene coding for transmembrane protein 240 (TMEM240) have been reported to be the causative mutations of spinocerebellar ataxia 21 (SCA21). We aimed to investigate the expression of TMEM240 ... ...

Abstract	A variety of missense mutations and a stop mutation in the gene coding for transmembrane protein 240 (TMEM240) have been reported to be the causative mutations of spinocerebellar ataxia 21 (SCA21). We aimed to investigate the expression of TMEM240 protein in mouse brain at the tissue, cellular, and subcellular levels. Immunofluorescence labeling showed TMEM240 to be expressed in various areas of the brain, with the highest levels in the hippocampus, isocortex, and cerebellum. In the cerebellum, TMEM240 was detected in the deep nuclei and the cerebellar cortex. The protein was expressed in all three layers of the cortex and various cerebellar neurons. TMEM240 was localized to climbing, mossy, and parallel fiber afferents projecting to Purkinje cells, as shown by co-immunostaining with VGLUT1 and VGLUT2. Co-immunostaining with synaptophysin, post-synaptic fractionation, and confirmatory electron microscopy showed TMEM240 to be localized to the post-synaptic side of synapses near the Purkinje-cell soma. Similar results were obtained in human cerebellar sections. These data suggest that TMEM240 may be involved in the organization of the cerebellar network, particularly in synaptic inputs converging on Purkinje cells. This study is the first to describe TMEM240 expression in the normal mouse brain.
MeSH term(s)	Adult ; Aged ; Animals ; Cerebellum/metabolism ; Cerebellum/pathology ; Gene Expression ; Humans ; Male ; Membrane Proteins/biosynthesis ; Membrane Proteins/genetics ; Mice ; Mice, Inbred C57BL ; Mutation/physiology ; Presynaptic Terminals/metabolism ; Presynaptic Terminals/ultrastructure ; Purkinje Cells/metabolism ; Purkinje Cells/ultrastructure ; Spinocerebellar Degenerations/genetics ; Spinocerebellar Degenerations/metabolism ; Spinocerebellar Degenerations/pathology ; Young Adult
Chemical Substances	Membrane Proteins ; TMEM240 protein, human
Language	English
Publishing date	2020-01-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	2112586-7
ISSN	1473-4230 ; 1473-4222
ISSN (online)	1473-4230
ISSN	1473-4222
DOI	10.1007/s12311-020-01112-y
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Zs.A 5795: Show issues

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Article: De la maladie de Pick aux démences fronto-temporales.

Pasquier, Florence / Deramecourt, Vincent / Lebert, Florence

Bulletin de l'Academie nationale de medecine

2012 Volume 196, Issue 2, Page(s) 431–42; discussion 442–3

Abstract: Frontotemporal dementias (FTD) are defined by a gradual change in social conduct, behavior and language, associated with frontal and anterior temporal lobe degeneration. The clinicalfeatures depend on the location of the degenerative process. In the last ...

Title translation	From Pick's disease to frontotemporal dementia.
Abstract	Frontotemporal dementias (FTD) are defined by a gradual change in social conduct, behavior and language, associated with frontal and anterior temporal lobe degeneration. The clinicalfeatures depend on the location of the degenerative process. In the last 20 years, increasingly specific and sensitive operational criteria have been established. Ongoing neuropathological and genetic studies have highlighted overlaps between FTD, motor neuron disease, and atypical parkinsonian syndromes (supranuclear palsy, corticobasal degeneration). They have also provided a better knowledge of the pathophysiology of FTD, and new specific therapeutic targets. These dementias, which usually occur before the age of 65 years, are now better recognized but are still underdiagnosed and often initially mistaken for psychiatric illnesses. Healthcare professionals managing these patients must therefore be better informed Serotonergic agents provide a symptomatic improvement, but environmental adaptation, prevention of language and swallowing difficulties, and information and support for the family and caregivers remain essential.
MeSH term(s)	Behavioral Symptoms/etiology ; Diagnosis, Differential ; Frontotemporal Dementia/diagnosis ; Frontotemporal Dementia/epidemiology ; Frontotemporal Dementia/genetics ; Frontotemporal Dementia/psychology ; Humans ; Pick Disease of the Brain/diagnosis ; Pick Disease of the Brain/epidemiology ; Pick Disease of the Brain/genetics ; Pick Disease of the Brain/psychology
Language	French
Publishing date	2012-02
Publishing country	Netherlands
Document type	English Abstract ; Journal Article
ZDB-ID	213227-8
ISSN	0001-4079
ISSN	0001-4079
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Article ; Online: Microvascular pathology and morphometrics of sporadic and hereditary small vessel diseases of the brain.

Craggs, Lucinda J L / Yamamoto, Yumi / Deramecourt, Vincent / Kalaria, Raj N

Brain pathology (Zurich, Switzerland)

2014 Volume 24, Issue 5, Page(s) 495–509

Abstract: Small vessel diseases (SVDs) of the brain are likely to become increasingly common in tandem with the rise in the aging population. In recent years, neuroimaging and pathological studies have informed on the pathogenesis of sporadic SVD and several ... ...

Abstract	Small vessel diseases (SVDs) of the brain are likely to become increasingly common in tandem with the rise in the aging population. In recent years, neuroimaging and pathological studies have informed on the pathogenesis of sporadic SVD and several single gene (monogenic) disorders predisposing to subcortical strokes and diffuse white matter disease. However, one of the limitations toward studying SVD lies in the lack of consistent assessment criteria and lesion burden for both clinical and pathological measures. Arteriolosclerosis and diffuse white matter changes are the hallmark features of both sporadic and hereditary SVDs. The pathogenesis of the arteriopathy is the key to understanding the differential progression of disease in various SVDs. Remarkably, quantification of microvascular abnormalities in sporadic and hereditary SVDs has shown that qualitatively the processes involved in arteriolar degeneration are largely similar in sporadic SVD compared with hereditary disorders such as cerebral autosomal arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). Important significant regional differences in lesion location within the brain may enable one to distinguish SVDs, where frontal lobe involvement appears consistently with almost every SVD, but others bear specific pathologies in other lobes, such as the temporal pole in CADASIL and the pons in pontine autosomal dominant microangiopathy and leukoencephalopathy or PADMAL. Additionally, degenerative changes in the vascular smooth muscle cells, the cerebral endothelium and the basal lamina are often rapid and more aggressive in genetic disorders. Further quantification of other microvascular elements and even neuronal cells is needed to fully characterize SVD pathogenesis and to differentiate the usefulness of vascular interventions and treatments on the resulting pathology.
MeSH term(s)	Age of Onset ; Brain/blood supply ; Brain/pathology ; CADASIL/pathology ; Cerebral Small Vessel Diseases/epidemiology ; Cerebral Small Vessel Diseases/genetics ; Cerebral Small Vessel Diseases/pathology ; Humans ; Microvessels/pathology
Language	English
Publishing date	2014-10-16
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1051484-3
ISSN	1750-3639 ; 1015-6305
ISSN (online)	1750-3639
ISSN	1015-6305
DOI	10.1111/bpa.12177
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