Evidence map›Paper›PMID 39167281›Full record

ArticleCell biochemistry and biophysics2025

Computational Identification and Functional Analysis of Potentially Pathogenic nsSNPs in the NLRP3 Gene Linked to Alzheimer's Disease.

Alya Redhwan, Mohd Adnan, Hadeel R Bakhsh, Nawaf Alshammari, Malvi Surti, Mansi Parashar, Mirav Patel, Mitesh Patel, Dinesh Sosalagere Manjegowda, Sameer Sharma

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Article in Cell biochemistry and biophysics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–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

3 citing papers in PubMed.

  1. Review
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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

10 authors.

Alya RedhwanDepartment of Health, College of Health and Rehabilitation Sciences, Princess Nourah bint Abdulrahman University, Riyadh, 11671, Saudi Arabia.
Mohd AdnanDepartment of Biology, College of Science, University of Ha'il, Ha'il, Saudi Arabia.
Hadeel R BakhshDepartment of Rehabilitation Sciences, College of Health and Rehabilitation Sciences, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia.
Nawaf AlshammariDepartment of Health, College of Health and Rehabilitation Sciences, Princess Nourah bint Abdulrahman University, Riyadh, 11671, Saudi Arabia.
Malvi Surti4Research and Development Cell, Department of Biotechnology, Parul Institute of Applied Sciences, Parul University, Vadodara, Gujarat, India.
Mansi Parashar4Research and Development Cell, Department of Biotechnology, Parul Institute of Applied Sciences, Parul University, Vadodara, Gujarat, India.
Mirav Patel4Research and Development Cell, Department of Biotechnology, Parul Institute of Applied Sciences, Parul University, Vadodara, Gujarat, India.
Mitesh Patel4Research and Development Cell, Department of Biotechnology, Parul Institute of Applied Sciences, Parul University, Vadodara, Gujarat, India.
Dinesh Sosalagere Manjegowda4Department of Human Genetics, School of Basic and Applied Sciences, Dayananda Sagar University, Bangalore, 560078, India.
Sameer SharmaDepartment of Bioinformatics, BioNome, Bangalore, India. sameer@bionome.in.

Funding

Princess Nourah Bint Abdulrahman University PNURSP2024R146
6 · The paper itself

Abstract

Single Nucleotide Polymorphisms (SNPs) are key in understanding complex diseases. Nonsynonymous single-nucleotide polymorphisms (nsSNPs) occur in protein-coding regions, potentially altering amino acid sequences, protein structure and function. Computational methods are vital for distinguishing deleterious nsSNPs from neutral ones. We investigated the role of NLRP3 gene in neuroinflammation associated with Alzheimer's disease (AD) pathogenesis. A total of 893 missense (nsSNPs) were obtained from the dbSNP database and subjected to rigorous filtering using bioinformatics tools like SIFT, Align GVGD, PolyPhen-2, and PANTHER to identify potentially damaging variants. Of these, 18 nsSNPs were consistently predicted to have deleterious effects across all tools. Notably, 16 of these variants exhibited reduced protein stability, while only 4 were predicted to be buried within the protein structure. Among the identified nsSNPs, rs180177442 (R262L and R262P), rs201875324 (T659I), and rs139814109 (T897M) were classified as high-risk variants due to their significant deleterious impact, probable damaging effects, and association with decreased protein stability. Molecular docking and simulation analyses were conducted utilizing Memantine, a standard drug utilized in AD treatment, to investigate potential interactions with the altered protein structures. Additional clinical and genetic investigations are necessary to elucidate the underlying mechanisms that link NLRP3 polymorphisms with the initiation of AD.

Indexed as

Alzheimer DiseaseComputational BiologyNLR Family, Pyrin Domain-Containing 3 ProteinPolymorphism, Single NucleotideHumansMolecular Docking SimulationProtein StabilityNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanAlzheimer’sdeleteriousNLRP3nsSNPSNP

Identifiers

PMID39167281

What Socratic holds

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Registered trials

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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.