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Microglia: Friend and foe in tauopathy
Open accessAbstract
Aggregation of misfolded microtubule associated protein tau into abnormal intracellular inclusions defines a class of neurodegenerative diseases known as tauopathies. The consistent spatiotemporal progression of tau pathology in Alzheimer's disease (AD) led to the hypothesis that tau aggregates spread in the brain via bioactive tau "seeds" underlying advancing disease course. Recent studies implicate microglia, the resident immune cells of the central nervous system, in both negative and positive regulation of tau pathology. Polymorphisms in genes that alter microglial function are associated with the development of AD and other tauopathies. Experimental manipulation of microglia function can alter tau pathology and microglia-mediated neuroinflammatory cascades can exacerbate tau pathology. Microglia also exert protective functions by mitigating tau spread: microglia internalize tau seeds and have the capacity to degrade them. However, when microglia fail to degrade these tau seeds there are deleterious consequences, including secretion of exosomes containing tau that can spread to neurons. This review explores the intersection of microglia and tau from the perspective of neuropathology, neuroimaging, genetics, transcriptomics, and molecular biology. As tau-targeted therapies such as anti-tau antibodies advance through clinical trials, it is critical to understand the interaction between tau and microglia.
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“The phagocytic activity of microglia is crucial for the removal of Aβ,94 tau,95 and α-synuclein.96”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [95]
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Metadata
- Authors
- Odfalk, K. F., Bieniek, K. F., & Hopp, S. C.
- Affiliations
- The University of Texas at San Antonio Health Science Center (US)
- Corresponding author
- Hopp, Sarah C.
- Venue
- Progress in Neurobiology
- Publisher
- Elsevier BV
- Published
- 2022-09
- Volume
- 216
- Pages
- 102306
- ISSN
- 0301-0082 (ISSN-L)
- PMC
- PMC9378545
- OpenAlex
- W4282841274
- Cited by
- 60
- References
- 265
- Citations by year
- 2026: 17 · 2025: 19 · 2024: 13 · 2023: 8 · 2022: 3
- FWCI
- 1.51
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (am, 480 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Progress in Neurobiology (acceptedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (K01AG066747, R21AG072423, R01AG062348, R01AG070214, P30AG066546)
- National Institute of Neurological Disorders and Stroke (T32NS082145, R01NS017950)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- microglia, tauopathy, tau aggregation, Alzheimer's disease, tau seeding, neuroinflammation, tau spread, exosomes, anti-tau antibodies, tau-targeted therapy
- MeSH terms
- Alzheimer Disease, Brain, Humans, Neurons, tau Proteins, Microglia, Tauopathies
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