Cited by 126Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsNeurological Disease Mechanisms and Treatments

Microglial priming in Alzheimer’s disease

Open access
Li, Jun-Wei, Zong, Yu, Cao, Xi-Peng, Tan, Lin, Tan, Lan·2018·Annals of Translational Medicine

Abstract

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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Crossref · 10.21037/atm.2018.04.22

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  • Growing body of evidence supports the involvement of the neuroimmune system, mast cells, and microglia in AD onset and progression.

    “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]

    The Introduction and Systemic inflammation dependent sections say that evidence links immune responses, neuroinflammation, and microglial activation to AD pathogenesis and progression. Our copy does not establish the claimed involvement of mast cells; a search for “mast cells” found no relevant passage. (LLM, conf=0.88)

    Experimental — accuracy not yet measured
  • Primed microglia can stimulate the release of Aβ and tau protein, leading to formation of neuritic plaques and neurofibrillary tangles, and reduce production of neurotrophic factors.

    “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].”

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2 of the 133 references couldn’t be matched to a known paper.

Research works printed but not linked: 1

  1. Guerreiro R, Hardy J. TREM2 and neurodegenerative disease. N Engl J Med 2013;369:1569-70.

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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
Published
2018-05
Volume
6
Issue
10
Pages
176-176
ISSN
  • 2305-5839 (ISSN-L)
  • 2305-5847
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
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
  • Health Sciences › Medicine › Physiology › 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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