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39/100

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Inflammation and the immune system

Topic: Amyloid, tau and blood-test diagnosis

Plain-language summary

Alzheimer's disease (AD), the most prevalent form of dementia, is pathologically defined by amyloid-β (Aβ) plaques, neurofibrillary tangles, synaptic loss, and progressive neuronal degeneration. Increasing evidence highlights neuroinflammation as a central and modifiable factor in AD pathogenesis. This review critically explores the roles of microglia and astrocytes in mediating neuroinflammatory cascades, emphasizing their dual protective and detrimental functions. Microglial activation and astrocytic polarization into A1 (neurotoxic) and A2 (neuroprotective) subtypes are discussed alongside their contributions to Aβ clearance, tau pathology propagation, and synaptic dysfunction. The disruption of the blood–brain barrier, activation of inflammasome pathways such as NLRP3, and release of cytokines and chemokines exacerbate chronic inflammation and neurodegeneration. Advances in single-cell transcriptomics and lipidomics have revealed glial heterogeneity and novel molecular targets, including disease-associated microglia. Genetic risk factors like apolipoprotein E ( APOE ) and TREM2 variants further modulate inflammatory responses. Emerging therapeutic strategies, including non-steroidal anti-inflammatory drugs, monoclonal antibodies, and targeted immunomodulators, hold promise for modifying disease progression. Overall, precise targeting of neuroinflammatory pathways offers a compelling avenue for future AD therapies.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Kakkar, A. K., Singh, H., Singh, B. K., Kumar, A., Mishra, A. K., & Chopra, H. (2025). Neuroinflammation and Alzheimer's disease: Unravelling the molecular mechanisms. Journal of Alzheimer s Disease. https://doi.org/10.1177/13872877251374353

Vancouver

Kakkar AK, Singh H, Singh BK, Kumar A, Mishra AK, Chopra H. Neuroinflammation and Alzheimer's disease: Unravelling the molecular mechanisms. Journal of Alzheimer s Disease. 2025. doi:10.1177/13872877251374353. PMID: 40938771.

BibTeX

@article{kakkar2025-40938771,
  author  = {Kakkar, A. K. and Singh, Harpreet and Singh, Bhuvnesh Kumar and Kumar, Arvind and Mishra, Arun Kumar and Chopra, Hitesh},
  title   = {{Neuroinflammation and Alzheimer's disease: Unravelling the molecular mechanisms}},
  journal = {Journal of Alzheimer s Disease},
  year    = {2025},
  doi     = {10.1177/13872877251374353},
  pmid    = {40938771},
  url     = {https://doi.org/10.1177/13872877251374353}
}

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How to read this study

Design: our record does not state a study design, so check the methods section of the original before weighing the result.
Size: the record gives no participant count. Look for one in the original before trusting a pattern.
Effect: the record gives no effect size, so the summary above cannot say how large any difference was.

What the evidence grade means here

This page is graded low. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Low means the abstract matched neither pattern. It is the default label, and it does not mean the work is poor; many sound lab and imaging papers land here. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

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Key findings

Advances in single-cell transcriptomics and lipidomics have revealed glial heterogeneity and novel molecular targets, including disease-associated microglia.
Overall, precise targeting of neuroinflammatory pathways offers a compelling avenue for future AD therapies.

Why it matters

This review describes neuroinflammation as a central and modifiable factor in Alzheimer's disease and discusses glial cells, genetic risk factors, and emerging therapeutic strategies. It suggests precise targeting of neuroinflammatory pathways as a future avenue but does not report a proven treatment.

Study details

Evidence strengthLow

How this study scored 39/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it. We have no data on senior author's track record, so that was left out: it earned 37 of the 96 points we could judge it on, which is 39 out of 100.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Journal of Alzheimer s Disease)
Journal's citation record	2 / 4	Journal of Alzheimer s Disease: journal h-index 218 (OpenAlex, 2026-10-29)
Study design	0 / 12	No study design recorded — scores zero, not guessed (not stated in the record — scored 0)
Strength of evidence	1 / 5	Rated “low” in our summary
Peer-review validation	10 / 10	Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent	4 / 5	2025 — within 3 year(s) of the newest study here
Sample size	0 / 4	Participant count not stated — scores zero (not stated in the record — scored 0)
Effect reported	0 / 3	No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people	0 / 3	Not stated whether this was studied in people — scores zero (not stated in the record — scored 0)
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	3 / 7	Cited 20 times (OpenAlex, 2026-10-10)
Citations per year	2 / 5	6.7 citations a year over 3 year(s) since 2025
Impact for its field and year	3 / 6	Cited 6.1× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	0 / 6	No other study in this library cites it
Still being cited	2 / 4	Cited 20 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	— / 4	Senior author's record not available — left out of this score
Institution's track record	0 / 3	Saveetha University: institution h-index 245 (OpenAlex)
Multicenter collaboration	1 / 3	OpenAlex lists 2 institution(s) in 1 country
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 40938771)
Free to read	0 / 2	Behind a paywall — scores zero
Points	37 / 96	Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 37 of the 96 points we could judge it on is 39 out of 100.
Total	39 / 100	—

What each of these 20 components measures, and what this score is not →

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