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Bouvier, D. S.

Publications and source records attributed to Bouvier, D. S..

4 recordsLinked to original sources

Disease-specific tangle immunophenotypes distinguish hippocampal vulnerability in Alzheimers disease and Parkinsons disease dementia

Structured AbstractINTRODUCTION Tau pathology typically occurs in Alzheime[r]s disease (AD), however is also frequently present in Parkinso[n]s disease dementia (PDD) and Dementia with Lewy Bodies (DLB), yet its disease-specific signature is unclear. METHODSFive tau, amyloid-{beta}, -synuclein and neuronal markers were analysed across hippocampal subfields in non-demented controls (CTLs), AD, PDD and DLB using multiplex immunohistochemistry, single-tangle classification and confocal imaging. RESULTSAT8, pTau217, and GT38 were predominatly detected in AD, while pS422 was enriched in PDD and pS396 showed a region- and disease-specific pattern. DLB resembled AD in subregional tau distribution. Tau marker correlation were different comparing AD, PDD and CTL. Single-tangle analyses revealed disease-specific immunophenotypes but conserved mature intra-tangle epitope organisation. Distinct tau signatures were associated with inhibitory interneuron vulnerability, while regional tau co-occurrence with amyloid-{beta} and -synuclein remained conserved. DISCUSSIONDisease-specific tau signatures vary across hippocampal subregions and neuronal populations, implicating the contribution of regional and cell-specific factors beyond pathology burden.

neuroscience↗

GPC5 expression highlights astrocytic heterogeneity and divergent hippocampal responses in Alzheimer's and Parkinson's Dementia

Regional heterogeneity of astrocytes and neurons is increasingly recognised as a determinant of selective vulnerability in neurodegeneration, yet the molecular signatures underlying this specificity remain poorly defined. Glypican-5 (GPC5), a heparan sulfate proteoglycan expressed mainly by astrocytes, contributes to synaptic organisation and circuit stability, whose disruption may undermine astrocyte-neuron crosstalk and contribute to selective neuronal loss in neurodegenerative diseases. Using multiplex chromogenic immunohistochemistry, in situ hybridization and digital pathology, we mapped GPC5 expression across the hippocampus and parahippocampal cortex in post-mortem tissue from non-demented control (CTL), Alzheimers disease (AD) and Parkinsons disease with dementia (PDD) cases. In CTL brains, GPC5 labelled spatially restricted populations of astrocytes and pyramidal neurons organized according to hippocampal subfield and laminar architecture. GPC5-positive astrocytes co-expressed canonical markers but represented a more restricted population while GPC5 protein was enriched at synapse-rich regions of the outer molecular layer of the dentate gyrus. In AD and PDD, regional distribution patterns of GPC5 were distinct from canonical astrocyte markers including GFAP, AQP4 and ALDH1L1. In PDD, GPC5 distribution was largely preserved. In AD, GPC5 underwent selective redistribution with a significant loss of the staining in the dentate gyrus, and an accumulation on amyloid plaques, putatively secreted by plaque-associated astrocytes, and on neurofibrillary tangles, likely of neuronal and astrocytic origin These findings reveal disease- and region-specific remodelling of a spatially organised astrocyte-neuron system and establish GPC5 as a molecularly distinct responder to AD pathology.

neuroscience↗

Concomitant AD and DLB pathologies shape subfield microglia responses in the hippocampus

Hippocampal alteration is at the centre of memory decline in the most common age-related neurodegenerative diseases: Alzheimers disease (AD) and Dementia with Lewy Bodies (DLB). However, the subregional deterioration of the hippocampus differs between both diseases with more severe atrophy in the CA1 subfield of the AD patients. How AD and DLB-typical pathologies compose the various local microenvironment of the hippocampus across AD and DLB needs to be further explored to understand this process. Additionally, microglia responses could further impact the atrophy rate. Some studies suggest that microglia react differently according to the underlying neurodegenerative disorder. How microglia are transformed across hippocampal subfields in AD and DLB, and how their changes are associated with disease-typical pathologies remains to be determined. To these purposes, we performed a volumetric analysis of phospho-Tau (P-Tau), Amyloid-{beta} (A{beta}), and phospho--Synuclein (P-Syn) loads, quantified and classified microglia according to distinct morphological phenotypes using high-resolution confocal 3D microscopy of hippocampal CA1, CA3 and DG/CA4 subfields of late-onset AD (n=10) and DLB (n=8) as well as age-matched control samples (n=11). We found that each of the Tau, A{beta} and Synuclein pathologies followed a specific subregional distribution, relatively preserved across AD and DLB. P-Tau, A{beta} and P-Syn burdens were significantly exacerbated in AD, with Tau pathology being particularly severe in the AD CA1. P-Tau and P-Syn burdens were highly correlated across subfields and conditions (R2Spear = 0.79; P < 0.001) and result from a local co-distribution of P-Tau and P-Syn inclusions in neighbouring neurons, with only a low proportion of double-positive cells. In parallel, we assessed the changes of the microglia responses by measuring 16 morphological features of more than 35,000 individual microglial cells and classifying them into seven-distinct morphological clusters. We found microglia features- and clusters-variations subfield- and condition-dependent. Two of the seven morphological clusters, with more amoeboid and less branched forms, were identified as disease-enriched and found to be further increased in AD. Interestingly, some microglial features or clusters were associated with one but more often with a combination of two pathologies in a subfield-dependent manner. In conclusion, our study shows a multimodal association of the hippocampal microglia responses with the co-occurrence, distribution and severity of AD and DLB pathologies. In DLB hippocampi, pathological imprint and microglia responses follow AD trends but with lesser severity. Our study suggests that the increased pathological burdens of P-Tau and P-Syn and associated microglia alterations are involved in a more severe deterioration of the CA1 in AD as compared to DLB.

neuroscience↗

MIC-MAC: High-throughput analysis of three-dimensional microglia morphology in mammalian brains

Microglia, the resident immune cells of the brain, exhibit complex and diverse phenotypes depending on their physiological context including brain regions and disease states. While single-cell RNA-sequencing has recently resolved this heterogeneity, it does not capture tissue and intercellular mechanisms. Our complementary imaging-based approach enables automatic 3D-morphology characterization and classification of thousands of individual microglia in situ and revealed species- and disease-specific morphological phenotypes in mouse and human brain samples.

neuroscience↗