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New insights on the role of microglia in synaptic pruning in health and disease
Open accessAbstract
Recent genome-wide association studies implicate microglia in Alzheimer's disease (AD) pathogenesis; however, their biological significance remains poorly understood. Synapse loss is a significant correlate of cognitive decline that serves as a critical hallmark of AD and other neurodegenerative diseases; however, mechanisms underlying synaptic vulnerability remain elusive. Emerging research on microglia function in the healthy brain is providing new insight into fundamental roles of microglia and immune molecules in brain wiring. Among their many roles, microglia prune developing synapses and regulate synaptic plasticity and function. Here, we review and discuss how this emerging work may provide new insight into how disruptions in microglia-synapse interactions could contribute to synapse loss and dysfunction, and consequently cognitive impairment, in AD.
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“Genome-wide association studies (GWAS) implicate microglia and complement-related pathways in AD (1).”
From Complement and microglia mediate early synapse loss in Alzheimer mouse models (2016) · cites this paper as [1]
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“The parallels between DAM and PAM support the concept that genes expressed during development are reactivated in aging and degeneration (Hong et al., 2016).”
From Developmental Heterogeneity of Microglia and Brain Myeloid Cells Revealed by Deep Single-Cell RNA Sequencing (2019) · cites this paper as Hong et al., 2016
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“The synapse loss in the hippocampus and association cortices is an early hallmark of AD and strongly correlates with cognitive impairment (Hong et al., 2016).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Hong et al., 2016
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Metadata
- Authors
- Hong, S., Dissing-Olesen, L., & Stevens, B.
- Affiliations
- Boston Children's Hospital (US)
- Corresponding author
- Stevens, Beth
- Venue
- Current Opinion in Neurobiology
- Publisher
- Elsevier BV
- Published
- 2016-02
- Volume
- 36
- Pages
- 128-134
- ISSN
- 0959-4388 (ISSN-L)
- PMC
- PMC5479435
- OpenAlex
- W2225188179
- Cited by
- 557
- References
- 79
- Citations by year
- 2026: 30 · 2025: 43 · 2024: 52 · 2023: 59 · 2022: 63 · 2021: 73 · 2020: 57 · 2019: 41 · 2018: 59 · 2017: 58 · 2016: 22
- FWCI
- 3.71
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Current Opinion in Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- Lundbeck Foundation
- Alzheimer's Research Trust
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Keywords
- microglia, synaptic pruning, Alzheimer's disease, synaptic loss, synaptic plasticity, cognitive impairment, neurodegeneration, brain development, neuroinflammation
- MeSH terms
- Alzheimer Disease, Animals, Brain, Disease Models, Animal, Humans, Neuronal Plasticity, Microglia, Genome-Wide Association Study
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