Evidence mapPaperPMID 40510290Full record

ReviewIBRO neuroscience reports2025

Effect of neuroinflammation on the progression of Alzheimer's disease and its significant ramifications for novel anti-inflammatory treatments.

Pritam Kamila, Koyel Kar, Sailee Chowdhury, Priyanka Chakraborty, Ria Dutta, Sowmiya S, Ankul Singh S, Bhupendra Gopalbhai Prajapati

Abstract readReview
In one paragraph

Review in IBRO neuroscience reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
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

33 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  13. Chrysin Ameliorated Neurochemical and Behavioural Changes Mediated By Combined Exposure of Interleukin-17 A With Amyloid BetaJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
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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

8 authors.

Pritam KamilaBCDA College of Pharmacy & Technology, Department of Pharmaceutical Chemistry, 78/1- Jessore Road (South), Hridaypur, Kolkata, West Bengal 700127, India.
Koyel KarBCDA College of Pharmacy & Technology, Department of Pharmaceutical Chemistry, 78/1- Jessore Road (South), Hridaypur, Kolkata, West Bengal 700127, India.
Sailee ChowdhuryBCDA College of Pharmacy & Technology, Department of Pharmaceutical Chemistry, 78/1- Jessore Road (South), Hridaypur, Kolkata, West Bengal 700127, India.
Priyanka ChakrabortyBCDA College of Pharmacy & Technology, Department of Pharmaceutical Chemistry, 78/1- Jessore Road (South), Hridaypur, Kolkata, West Bengal 700127, India.
Ria DuttaBCDA College of Pharmacy & Technology, Department of Pharmaceutical Chemistry, 78/1- Jessore Road (South), Hridaypur, Kolkata, West Bengal 700127, India.
Sowmiya SDepartment of Pharmacology, Faculty of Pharmacy, Dr. M.G.R Educational and Research Institute, Velappanchavadi, Chennai, Tamil Nadu 600077, India.
Ankul Singh SDepartment of Pharmacology, Faculty of Pharmacy, Dr. M.G.R Educational and Research Institute, Velappanchavadi, Chennai, Tamil Nadu 600077, India.
Bhupendra Gopalbhai PrajapatiShree S.K. Patel College of Pharmaceutical Education & Research, Ganpat University, Kherva, Mehsana, Gujarat 384012, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is increasingly recognized as a disorder not solely of amyloid and tau accumulation but also of chronic immune dysregulation. Emerging evidence highlights the critical role of neuroinflammation, characterized by sustained activation of microglia and astrocytes, cytokine release, and inflammasome activation in accelerating AD progression. Genome-wide studies have further identified key inflammatory genes and immune pathways associated with increased disease risk. This review critically evaluates the mechanistic underpinnings of neuroinflammation in AD, focusing on glial cell behavior, immune signaling, and their contribution to neuronal dysfunction. Importantly, the review highlights recent advances in anti-inflammatory therapeutic approaches, including modulators of IL-1β, TNF-α, TREM2, and CB2 pathways. By integrating mechanistic and therapeutic insights, this work underscores the potential of immunomodulatory strategies as viable interventions in AD and provides a novel framework for future research in targeted anti-neuroinflammatory treatments.

Indexed as

Alzheimer’s diseaseAnti-inflammatory therapyCytokinesGlial cellsMicrogliaNeuroinflammation

Identifiers

PMID40510290
PMCPMC12159511

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.