The DOI matches its Crossref record; 131 of the 133 references it cites were found in a registry or an index.
Microglial priming in Alzheimer’s disease
Open accessAbstract
Alzheimer's disease (AD) is a chronic and progressive neurodegenerative disease of central nervous system (CNS). Nowadays, increasing evidence suggests that immune system plays a significant role in the mechanisms of AD's onset and progression. Microglia, the main participator in the immune system of CNS, is always regarded as a protector of our brain in a healthy state and also has a beneficial role in maintaining the homeostasis of CNS microenvironment. However, chronic and sustained stimulation can push microglia into the state termed priming. Primed microglia can induce the production of amyloid β (Aβ), tau pathology, neuroinflammation and reduce the release of neurotrophic factors, resulting in loss of normal neurons in quantity and function that has immense relationship with AD. The therapeutic strategies mainly aimed at modulating the microenvironment and microglial activity in CNS to delay progression and alleviate pathogenesis of AD. Overall, in this review, we highlight the mechanism of microglial priming, and discuss the profound relationship between microglial priming and AD. Besides, we also pay attention to the therapeutic strategies targeting at microglial priming.
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“The effort to find an innovative non-amyloid-based compound acting on neuroinflammation could be another treatment option since the growing body of evidence supports the involvement of the neuroimmune system, mast cells (MCs), and microglia in AD onset and progression [125,126].”
From Treatment of Alzheimer’s Disease: Beyond Symptomatic Therapies (2023) · cites this paper as [125]
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“Primed microglia can stimulate the release of Aβ and tau protein with the following formation of neuritic plaques and neurofibrillary tangles, as well as reducing the production of neurotrophic factors [125].”
From Treatment of Alzheimer’s Disease: Beyond Symptomatic Therapies (2023) · cites this paper as [125]
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Metadata
- Authors
- Li, J.-W., Zong, Y., Cao, X.-P., Tan, L., & Tan, L.
- Affiliations
- Qingdao University (CN)
- Corresponding author
- Tan, Lin
- Tan, Lan
- Venue
- Annals of Translational Medicine
- Publisher
- AME Publishing Company
- Published
- 2018-05
- Volume
- 6
- Issue
- 10
- Pages
- 176-176
- ISSN
- 2305-5839 (ISSN-L)
- 2305-5847
- PMC
- PMC5994530
- OpenAlex
- W2800869030
- Cited by
- 122
- References
- 133
- Citations by year
- 2026: 8 · 2025: 11 · 2024: 26 · 2023: 22 · 2022: 13 · 2021: 18 · 2020: 13 · 2019: 9 · 2018: 2
- FWCI
- 0.99
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc-nd
- Locations
- Annals of Translational Medicine (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Qingdao Key Health Discipline Development Fund
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- Alzheimer's disease, microglial priming, microglia, neuroinflammation, amyloid-beta, tau pathology, neurotrophic factors, neurodegeneration
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