Evidence map›Paper›PMID 29951498›Full record

ReviewAnnals of translational medicine2018

Microglial priming in Alzheimer's disease.

Jun-Wei Li, Yu Zong, Xi-Peng Cao, Lin Tan, Lan Tan

Abstract readReview
In one paragraph

Review in Annals of translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

71 citing papers in PubMed.

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  19. Rejuvenating aged microglia by p16Molecular neurodegeneration · 2024
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11 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Jun-Wei LiDepartment of Neurology, Qingdao Municipal Hospital, Dalian Medical University, Qingdao 266000, China.
Yu ZongDepartment of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao 266071, China.
Xi-Peng CaoClinical Research Center, Qingdao Municipal Hospital, Qingdao University, Qingdao 266071, China.
Lin TanDepartment of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao 266071, China.
Lan TanDepartment of Neurology, Qingdao Municipal Hospital, Dalian Medical University, Qingdao 266000, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Alzheimer’s disease (AD)amyloid beta (Aβ)microglial primingneuroinflammationtau-protein

Identifiers

PMID29951498
PMCPMC5994530

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.