Evidence map›Paper›PMID 36006570›Full record

ReviewInflammation2023

Role of NLRP3 Inflammasome and Its Inhibitors as Emerging Therapeutic Drug Candidate for Alzheimer's Disease: a Review of Mechanism of Activation, Regulation, and Inhibition.

Barkha Sharma, Garvit Satija, Anish Madan, Mansi Garg, M Mumtaz Alam, M Shaquiquzzaman, Suruchi Khanna, Prachi Tiwari, Suhel Parvez, Ashif Iqubal and 2 more

Open access · bronzeAbstract readReview
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 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.9field-weighted citation impact, top 3% 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

42 citing papers in PubMed, 63 citations in OpenAlex.

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  13. The Ubiquitin-Proteasome System in Brain Disorders: Pathogenic Pathways, Post-Translational Tweaks, and Therapeutic Frontiers.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
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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

12 authors at 1 institution in 1 country.

Barkha Sharma *Drug Design and Medicinal Chemistry Lab, Department of Pharmaceutical Chemistry, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, India.
Garvit Satija *Drug Design and Medicinal Chemistry Lab, Department of Pharmaceutical Chemistry, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, India.
Anish MadanDrug Design and Medicinal Chemistry Lab, Department of Pharmaceutical Chemistry, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, India.
Mansi GargDrug Design and Medicinal Chemistry Lab, Department of Pharmaceutical Chemistry, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, India.
M Mumtaz AlamDrug Design and Medicinal Chemistry Lab, Department of Pharmaceutical Chemistry, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, India.
M ShaquiquzzamanDrug Design and Medicinal Chemistry Lab, Department of Pharmaceutical Chemistry, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, India.
Suruchi KhannaDepartment of Pharmacology, Shambhunath Institute of Pharmacy (Affiliated to AKTU), Prayagraj, UP-211012, India.
Prachi TiwariDepartment of Rehabilitation Sciences, School of Nursing Sciences and Allied Health, Jamia Hamdard, New Delhi, India.
Suhel ParvezDepartment of Toxicology, School of Chemical and Life Sciences, Jamia Hamdard, New Delhi, India.
Ashif IqubalDepartment of Pharmacology, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, India. asifiqubal2013@gmail.com.
Syed Ehtaishamul HaqueDepartment of Pharmacology, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, India.
Mohammad Ahmed KhanDepartment of Pharmacology, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, India. khan.ahmed1511@gmail.com.
Jamia Hamdard · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is one of the most prevalent neurodegenerative disorders. The etiology and pathology of AD are complicated, variable, and yet to be completely discovered. However, the involvement of inflammasomes, particularly the NLRP3 inflammasome, has been emphasized recently. NLRP3 is a critical pattern recognition receptor involved in the expression of immune responses and has been found to play a significant role in the development of various immunological and neurological disorders such as multiple sclerosis, ulcerative colitis, gout, diabetes, and AD. It is a multimeric protein which releases various cytokines and causes caspase-1 activation through the process known as pyroptosis. Increased levels of cytokines (IL-1β and IL-18), caspase-1 activation, and neuropathogenic stimulus lead to the formation of proinflammatory microglial M1. Progressive researches have also shown that besides loss of neurons, the pathophysiology of AD primarily includes amyloid beta (Aβ) accumulation, generation of oxidative stress, and microglial damage leading to activation of NLRP3 inflammasome that eventually leads to neuroinflammation and dementia. It has been suggested in the literature that suppressing the activity of the NLRP3 inflammasome has substantial potential to prevent, manage, and treat Alzheimer's disease. The present review discusses the functional composition, various models, signaling molecules, pathways, and evidence of NLRP3 activation in AD. The manuscript also discusses the synthetic drugs, their clinical status, and projected natural products as a potential therapeutic approach to manage and treat NLRP3 mediated AD.

Indexed as

Alzheimer DiseaseInflammasomesAmyloid beta-PeptidesCaspasesCytokinesHumansNLR Family, Pyrin Domain-Containing 3 ProteinAmyloid beta-PeptidesCaspasesCytokinesInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinAlzheimer’s diseaseInflammasomeInflammationNLRP3

Identifiers

PMID36006570
PMCPMC9403980
OpenAlexW4293051919

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.