Evidence map›Paper›PMID 37932959›Full record

ReviewJournal of neurochemistry2024

Diverse signaling mechanisms and heterogeneity of astrocyte reactivity in Alzheimer's disease.

Hongwei Qin, Lianna Zhou, Faris T Haque, Cynthia Martin-Jimenez, Amy Trang, Etty N Benveniste, Qin Wang

Abstract readReview
In one paragraph

Review in Journal of neurochemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Review
  2. Article
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  4. Article
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  7. Review
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

7 authors.

Hongwei QinDepartment of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, Alabama, USA.ORCID 0000-0002-7511-5078
Lianna ZhouDepartment of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Faris T HaqueDepartment of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Cynthia Martin-JimenezDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia at Augusta University, Augusta, Georgia, USA.
Amy TrangDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia at Augusta University, Augusta, Georgia, USA.
Etty N BenvenisteDepartment of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Qin WangDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia at Augusta University, Augusta, Georgia, USA.

Funding

Project 3: LRRK2 mediated macrophage responses in PDP50NS108675 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI STANDAERT, DAVID G. · 2018 to 2022
$9.9M
Astrocytic OSMR/JAK/STAT signaling in ADR01AG075057 · NIA · AUGUSTA UNIVERSITY · PI Hongwei Qin, Qin Wang · 2023 to 2026
$2.5M
Beta amyloid-adrenergic receptor interaction in Alzheimer's DiseaseR01AG064664 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WANG, QIN · 2019 to 2024
$2.1M
Alpha2 adrenergic signaling in AD pathogenesisRF1AG056815 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WANG, QIN · 2018 to 2018
$2.0M
Regulation of SORLA by beta-arrestin2RF1AG067729 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WANG, QIN · 2020 to 2020
$2.0M
Regulation of SORLA by beta-arrestin2R01AG067729 · NIA · AUGUSTA UNIVERSITY · PI WANG, QIN · 2024 to 2024
$529k
NIA NIH HHS R01 AG064664NIA NIH HHS R01 AG067729NIA NIH HHS R01 AG075057NIA NIH HHS RF1 AG056815NIA NIH HHS RF1 AG067729NIH HHS AG064664NIH HHS AG067729NIH HHS AG075057NIH HHS NS108675NINDS NIH HHS P50 NS108675
6 · The paper itself

Abstract

Alzheimer's disease (AD) affects various brain cell types, including astrocytes, which are the most abundant cell types in the central nervous system (CNS). Astrocytes not only provide homeostatic support to neurons but also actively regulate synaptic signaling and functions and become reactive in response to CNS insults through diverse signaling pathways including the JAK/STAT, NF-κB, and GPCR-elicited pathways. The advent of new technology for transcriptomic profiling at the single-cell level has led to increasing recognition of the highly versatile nature of reactive astrocytes and the context-dependent specificity of astrocyte reactivity. In AD, reactive astrocytes have long been observed in senile plaques and have recently been suggested to play a role in AD pathogenesis and progression. However, the precise contributions of reactive astrocytes to AD remain elusive, and targeting this complex cell population for AD treatment poses significant challenges. In this review, we summarize the current understanding of astrocyte reactivity and its role in AD, with a particular focus on the signaling pathways that promote astrocyte reactivity and the heterogeneity of reactive astrocytes. Furthermore, we explore potential implications for the development of therapeutics for AD. Our objective is to shed light on the complex involvement of astrocytes in AD and offer insights into potential therapeutic targets and strategies for treating and managing this devastating neurodegenerative disorder.

Indexed as

Alzheimer DiseaseAstrocytesSignal TransductionAnimalsHumansAlzheimer's diseaseGPCR pathwayJAK/STAT pathwayNF‐κB pathwayreactive astrocytessignaling pathways

Identifiers

PMID37932959
PMCPMC11839148

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.