ArticleMolecular neurobiology2025
Association of MTHFR C677T and A1298C Polymorphisms in Metabolic Alterations, Neuroimaging, and Cognitive Decline in Alzheimer's Disease: Case-Control and Bioinformatics Insights.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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Who cites it
3 citing papers in PubMed.
- Regulation of NLRP3 inflammasome signaling in Alzheimer's disease: emerging neuroprotective role of phytochemicals.Inflammopharmacology · 2026Review
- Decoding neuroinflammation: the critical role of NLRP3 inflammasome in Alzheimer's disease.Inflammopharmacology · 2026Review
- Ganaxolone as a promising therapeutic agent for Alzheimer's disease: signaling pathways and mechanistic insights-a narrative review.Inflammopharmacology · 2026Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder influenced by genetic, metabolic, and lifestyle factors. Polymorphisms in the methylenetetrahydrofolate reductase (MTHFR) gene, notably C677T and A1298C, may increase AD susceptibility through disruptions in one-carbon metabolism and homocysteine accumulation. This study examined the association of MTHFR C677T and A1298C variants with metabolic alterations, cognitive decline, and AD risk. A case-control study was conducted with 120 AD patients and 120 cognitively healthy controls. Cognitive function was assessed using the Hindi Mini-Mental State Examination (HMMSE) and Hindi Mattis Dementia Rating Scale (HMDRS). MRI evaluated white matter hyperintensities and cortical atrophy. Biochemical markers, including homocysteine, folate, and vitamin B12, were measured. Genotyping was performed via TaqMan SNP assays. Functional enrichment and protein-protein interaction analyses were conducted to investigate molecular mechanisms. AD cases demonstrated elevated homocysteine and blood glucose, reduced folate, and impaired cognition. Both MTHFR C677T and A1298C polymorphisms were significantly associated with AD risk under dominant and over-dominant models (ORs 3.41-4.09). Risk-allele carriers exhibited pronounced metabolic alterations. Bioinformatics analyses revealed disruption in one-carbon metabolism, oxidative stress defense, and vascular pathways, with indirect interactions between MTHFR and key AD genes (APP, PSEN1/2, MAPT, APOE, CLU, PICALM, SORL1). MTHFR C677T and A1298C variants contribute to AD susceptibility through metabolic and vascular mechanisms that exacerbate cognitive decline. Integrating genetic, biochemical, and cognitive assessments highlights potential targets for early prevention and therapeutic interventions.
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Identifiers
41417174What Socratic holds
Registered trials
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.