Evidence map›Paper›PMID 35986874›Full record

ReviewInflammation2023

Neuroinflammation in Alzheimer's Disease: Current Progress in Molecular Signaling and Therapeutics.

Sujata Thakur, Rishika Dhapola, Phulen Sarma, Bikash Medhi, Dibbanti HariKrishna Reddy

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 315 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
315citing papers in PubMed, 3 pooled it
49.9field-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

315 citing papers in PubMed, 3 syntheses or guidelines pooled it, 458 citations in OpenAlex.

  1. Pooled it
  2. Efficacy and possible mechanism ofFrontiers in pharmacology · 2026
    Pooled it
  3. Pooled it
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Anatomy of a Setback: A Taxonomy of Clinical Trial Failures in Alzheimer's Disease and Strategic Lessons for the Future.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  14. Article
  15. Review
  16. Article
  17. Mechanisms, Biomarkers and Therapeutic Implications of Neuroinflammation in Alzheimer's Disease.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2026
    Review
  18. Review
  19. Article
  20. Review

255 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 at 3 institutions in 1 country.

Sujata ThakurDepartment of Pharmacology, Central University of Punjab, Bathinda, 151401, India.
Rishika DhapolaDepartment of Pharmacology, Central University of Punjab, Bathinda, 151401, India.
Phulen SarmaDepartment of Pharmacology, All India Institute of Medical Sciences, Mangalagiri, 522503, Andhra Pradesh, India.
Bikash MedhiDepartment of Pharmacology, Post Graduate Institute of Medical Education and Research, Chandigarh, 160 012, India.
Dibbanti HariKrishna ReddyDepartment of Pharmacology, Central University of Punjab, Bathinda, 151401, India. harikrishnareddy0011@gmail.com.
Central University of Punjab · INAll India Institute of Medical Sciences · INPost Graduate Institute of Medical Education and Research · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease, a neurodegenerative disease with amyloid beta accumulation as a major hallmark, has become a dire global health concern as there is a lack of clear understanding of the causative agent. It is a major cause of dementia which is increasing exponentially with age. Alzheimer's disease is marked by tau hyperphosphorylation and amyloid beta accumulation that robs people of their memories. Amyloid beta deposition initiated a spectrum of microglia-activated neuroinflammation, and microglia and astrocyte activation elicited expressions of various inflammatory and anti-inflammatory cytokines. Neuroinflammation is one of the cardinal features of Alzheimer's disease. Pro-inflammatory cytokine signaling plays multifarious roles in neurodegeneration and neuroprotection. Induction of proinflammatory signaling leads to discharge of immune mediators which affect functions of neurons and cause cell death. Sluggish anti-inflammatory system also contributes to neuroinflammation. Numerous pathways like NFκB, p38 MAPK, Akt/mTOR, caspase, nitric oxide, and COX are involved in triggering brain immune cells like astrocytes and microglia to secrete inflammatory cytokines such as tumor necrosis factor, interleukins, and chemokines and participate in Alzheimer's disease pathology. PPAR-γ agonists tend to boost the phagocytosis of amyloid beta and decrease the inflammatory cytokine IL-1β. Recent findings suggest the cross-link between gut microbiota and neuroinflammation contributing in AD which has been explained in this study. The role of cellular, molecular pathways and involvement of inflammatory mediators in neuroinflammation has also been described; targeting them could be a potential therapeutic strategy for treatment of AD.

Indexed as

Alzheimer DiseaseNeurodegenerative DiseasesAmyloid beta-PeptidesAnti-Inflammatory AgentsCytokinesHumansMicrogliaNeuroinflammatory DiseasesAmyloid beta-PeptidesAnti-Inflammatory AgentsCytokinesalzheimer’s diseasecytokinesgut microbiotainterleukinsmicroglianeuroinflammation

Identifiers

PMID35986874
OpenAlexW4294094040

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.