Microglia modulate neurodegeneration in Alzheimer’s and Parkinson’s diseases
Open accessAbstract
Dementia is a rapidly rising global health crisis that silently disables families and ends lives and livelihoods around the world. To date, however, no early biomarkers or effective therapies exist. It is now clear that brain microglia are more than mere bystanders or amyloid phagocytes; they can act as governors of neuronal function and homeostasis in the adult brain. Here, we highlight the fundamental role of microglia as tissue-resident macrophages in neuronal health. Then, we suggest how chronic impairment in microglia-neuron cross-talk may secure the permanence of the failure of synaptic and neuronal function and health in Alzheimer’s and Parkinson’s diseases. Understanding how to assess and modulate microglia-neuron interactions critical for brain health will be key to developing effective therapies for dementia.
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The uptake and processing of non-toxic α-syn by glia could lead to the generation of toxic strains specific to the disease through autophagy and impaired lysosomal degradation.
“The uptake and processing of non-toxic α-syn by glia could lead to the generation of toxic strains specific to the disease through autophagy and impaired lysosomal degradation250”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [250]
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- Authors
- Bartels, T., De Schepper, S., & Hong, S.
- Affiliations
- UK Dementia Research Institute (GB)
- UK Dementia Research Institute, Institute of Neurology, University College London, London WC1E 6BT, UK.
- Corresponding author
- Hong, Soyon
- Venue
- Science
- Published
- 2020-10-02
- Volume
- 370
- Issue
- 6512
- Pages
- 66-69
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W3090922258
- Cited by
- 412
- References
- 70
- Citations by year
- 2026: 48 · 2025: 85 · 2024: 68 · 2023: 69 · 2022: 75 · 2021: 66 · 2020: 1
- FWCI
- 5.28
- Type
- journal article
- Language
- en
- Open access
- green
- discovery.ucl.ac.uk
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke
- Michael J. Fox Foundation for Parkinson's Research
- Parkinson's Disease Foundation
- Chan Zuckerberg Initiative
- Dementia Research UK
- UK Medical Research Council
- Alzheimer's Research UK
- Alzheimer's Society UK
- Eisai
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- microglia, neurodegeneration, Alzheimer's disease, Parkinson's disease, dementia, microglia-neuron interaction, tissue-resident macrophages, synaptic dysfunction, neuronal health, neuroinflammation
- MeSH terms
- Alzheimer Disease, Amyloid, Animals, Cell Communication, Humans, Macrophages, Neurons, Parkinson Disease, Synapses, Synaptosomes, Microglia, Mice, alpha-Synuclein
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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