Evidence map›Paper›PMID 34813026›Full record

ReviewInflammopharmacology2021

Recent advances in molecular pathways and therapeutic implications targeting neuroinflammation for Alzheimer's disease.

Rishika Dhapola, Subhendu Shekhar Hota, Phulen Sarma, Anusuya Bhattacharyya, Bikash Medhi, Dibbanti HariKrishna Reddy

Open access · bronzeAbstract readReview
In one paragraph

Review in Inflammopharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 205 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
205citing papers in PubMed, 6 pooled it
18.5field-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

205 citing papers in PubMed, 6 syntheses or guidelines pooled it, 338 citations in OpenAlex.

  1. Efficacy and possible mechanism ofFrontiers in pharmacology · 2026
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145 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

6 authors at 3 institutions in 1 country.

Rishika DhapolaDepartment of Pharmacology, Central University of Punjab, Bathinda, 151 401, India.
Subhendu Shekhar HotaDepartment of Pharmacology, Central University of Punjab, Bathinda, 151 401, India.
Phulen SarmaDepartment of Pharmacology, Post Graduate Institute of Medical Education and Research, Chandigarh, 160 012, India.
Anusuya BhattacharyyaDepartment of Ophthalmology, Government Medical College & Hospital, Chandigarh, 160 032, 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, 151 401, India. harikrishnareddy0011@gmail.com.ORCID http://orcid.org/0000-0003-2616-0195
Central University of Punjab · INPost Graduate Institute of Medical Education and Research · INGovernment Medical College and Hospital · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a major contributor of dementia leading to the degeneration of neurons in the brain with major symptoms like loss of memory and learning. Many evidences suggest the involvement of neuroinflammation in the pathology of AD. Cytokines including TNF-α and IL-6 are also found increasing the BACE1 activity and expression of NFκB resulting in generation of Aβ in AD brain. Following the interaction of Aβ with microglia and astrocytes, other inflammatory molecules also get translocated to the site of inflammation by chemotaxis and exaggerate neuroinflammation. Various pathways like NFκB, p38 MAPK, Akt/mTOR, caspase, nitric oxide and COX trigger microglia to release inflammatory cytokines. PPARγ agonists like pioglitazone increases the phagocytosis of Aβ and reduces inflammatory cytokine IL-1β. Celecoxib and roficoxib like selective COX-2 inhibitors also ameliorate neuroinflammation. Non-selective COX inhibitor indomethacin is also potent inhibitor of inflammatory mediators released from microglia. Mitophagy process is considered quite helpful in reducing inflammation due to microglia as it promotes the phagocytosis of over activated microglial cells and other inflammatory cells. Mitophagy induction is also beneficial in the removal of damaged mitochondria and reduction of infiltration of inflammatory molecules at the site of accumulation of the damaged mitochondria. Targeting these pathways and eventually ameliorating the activation of microglia can mitigate neuroinflammation and come out as a better therapeutic option for the treatment of Alzheimer's disease.

Indexed as

Molecular Targeted TherapyAlzheimer DiseaseAnimalsCytokinesHumansInflammationInflammation MediatorsMitochondriaMitophagyNeuroinflammatory DiseasesCytokinesInflammation MediatorsAlzheimer’s diseaseMolecular pathwaysNeuroinflammationTherapeutics

Identifiers

PMID34813026
PMCPMC8608577
OpenAlexW3215739089

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.