All roads lead to heterogeneity: The complex involvement of astrocytes and microglia in the pathogenesis of Alzheimer’s disease

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dc.contributor.authorSt-Pierre, Marie-Kim
dc.contributor.authorVanderZwaag, Jared
dc.contributor.authorLoewen, Sophia
dc.contributor.authorTremblay, Marie-Ève
dc.date.accessioned2024-02-09T23:01:48Z
dc.date.available2024-02-09T23:01:48Z
dc.date.copyright2022en_US
dc.date.issued2022
dc.description.abstractIn recent years, glial cells have been acknowledged as key players in the pathogenesis of Alzheimer’s disease (AD), a neurodegenerative condition in which an accumulation of intracellular neurofibrillary tangles and extracellular fibrillar amyloid beta is notably observed in the central nervous system. Genome-wide association studies have shown, both in microglia and astrocytes, an increase in gene variants associated with a higher risk of developing late-onset AD. Microglia, the resident innate immune cells of the brain, and astrocytes, glial cells crucial for vascular integrity and neuronal support, both agglomerate near amyloid beta plaques and dystrophic neurites where they participate in the elimination of these harmful parenchymal elements. However, their role in AD pathogenesis has been challenging to resolve due to the highly heterogeneous nature of these cell populations, i.e., their molecular, morphological, and ultrastructural diversity, together with their ever-changing responsiveness and functions throughout the pathological course of AD. With the recent expansions in the field of glial heterogeneity through innovative advances in state-of-the-art microscopy and -omics techniques, novel concepts and questions arose, notably pertaining to how the diverse microglial and astrocytic states interact with each other and with the AD hallmarks, and how their concerted efforts/actions impact the progression of the disease. In this review, we discuss the recent advances and findings on the topic of glial heterogeneity, particularly focusing on the relationships of these cells with AD hallmarks (e.g., amyloid beta plaques, neurofibrillary tangles, synaptic loss, and dystrophic neurites) in murine models of AD pathology and post-mortem brain samples of patients with AD.en_US
dc.description.reviewstatusRevieweden_US
dc.description.scholarlevelFacultyen_US
dc.description.sponsorshipM-KS-P was supported by doctoral training awards from the Canadian Institutes of Health Research (CIHR) and Fonds de recherche du Québec—Santé. JV holds a CIHR master’s training award. M-ÈT holds a Canada Research Chair (Tier 2) in Neurobiology of Aging and Cognition.en_US
dc.identifier.citationSt-Pierre, M-K., VanderZwaag, J., Loewen, S., & Tremblay, M-È. (2022). All roads lead to heterogeneity: The complex involvement of astrocytes and microglia in the pathogenesis of Alzheimer’s disease. Frontiers in Cellular Neuroscience, 16, 932572. https://doi.org/10.3389/fncel.2022.932572en_US
dc.identifier.urihttps://doi.org/10.3389/fncel.2022.932572
dc.identifier.urihttp://hdl.handle.net/1828/15983
dc.language.isoenen_US
dc.publisherFrontiers in Cellular Neuroscienceen_US
dc.subjectAlzheimer's diseaseen_US
dc.subjectheterogeneityen_US
dc.subjectmicrogliaen_US
dc.subjectastrocyteen_US
dc.subjectmurine modelen_US
dc.subjecthuman brain samplesen_US
dc.titleAll roads lead to heterogeneity: The complex involvement of astrocytes and microglia in the pathogenesis of Alzheimer’s diseaseen_US
dc.typeArticleen_US

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