Evidence map›Paper›PMID 30874945›Full record

ReviewInflammopharmacology2019

Activation of microglia and astrocytes: a roadway to neuroinflammation and Alzheimer's disease.

Darshpreet Kaur, Vivek Sharma, Rahul Deshmukh

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammopharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 257 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
257citing papers in PubMed, 2 pooled it
26.8field-weighted citation impact, top 1% of its field
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

257 citing papers in PubMed, 2 syntheses or guidelines pooled it, 472 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Review
  6. Excitation-inhibition imbalance links amyloid pathophysiology to cognition in non-demented individuals.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  7. Review
  8. Article
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  12. The bidirectional mechanistic links between Alzheimer's disease and cardiovascular disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Review
  13. Article
  14. Review
  15. Native PLGA nanoparticles attenuate disease pathology via multiple pathways in 5xFAD Alzheimer's model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
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  17. Article
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  20. Article

197 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

3 authors at 2 institutions in 1 country.

Darshpreet KaurDepartment of Pharmaceutical Sciences and Technology, Maharaja Ranjit Singh Punjab Technical University, Bathinda, Punjab, 151001, India.
Vivek SharmaGovernment College of Pharmacy, Rohru, Shimla, Himachal Pradesh, 171207, India.
Rahul DeshmukhDepartment of Pharmaceutical Sciences and Technology, Maharaja Ranjit Singh Punjab Technical University, Bathinda, Punjab, 151001, India. drrahuld09@gmail.com.ORCID http://orcid.org/0000-0001-5834-0962
Maharaja Ranjit Singh Punjab Technical University · INGovernment of Himachal Pradesh · IN

Funding

Science and Engineering Research Board SB/YS/LS-111/2013
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disease that is of high importance to the neuroscience world, yet the complex pathogenicity is not fully understood. Inflammation is usually observed in AD and could implicate both beneficial or detrimental effects depending on the severity of the disease. During initial AD pathology, microglia and astrocyte activation is beneficial since they are involved in amyloid-beta clearance. However, with the progression of the disease, activated microglia elicit detrimental effects by the overexpression of pro-inflammatory cytokines such as interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α) bringing forth neurodegeneration in the surrounding brain regions. This results in decline in Aβ clearance by microglia; Aβ accumulation thus increases in the brain resulting in neuroinflammation. Thus, Aβ accumulation is the effect of increased release of pro-inflammatory molecules. Reactive astrocytes acquire gain of toxic function and exhibits neurotoxic effects with loss of neurotrophic functions. Astrocyte dysfunctioning results in increased release of cytokines and inflammatory mediators, neurodegeneration, decreased glutamate uptake, loss of neuronal synapses, and ultimately cognitive deficits in AD. We discuss the role of intracellular signaling pathways in the inflammatory responses produced by astrocytes and microglial activation, including the glycogen synthase kinase-3β, nuclear factor kappa B cascade, mitogen-activated protein kinase pathways and c-Jun N-terminal kinase. In this review, we describe the role of neuroinflammation in the chronicity of AD pathogenesis and an overview of the recent research towards the development of new therapies to treat this disorder.

Indexed as

Alzheimer DiseaseAnimalsAstrocytesHumansInflammationMicrogliaNeuronsNeurotoxicity SyndromesSignal TransductionAlzheimer’s diseaseAstrocytesMicrogliaNeuroinflammationNeuronal synapsesPro-inflammatory cytokines

Identifiers

PMID30874945
OpenAlexW2921781039

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.