ArticleMolecular neurobiology2021
High Expression of Nicotinamide N-Methyltransferase in Patients with Sporadic Alzheimer's Disease.
Article in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Pharmacokinetic and pharmacodynamic assessment of oral nicotinamide in the NEAT clinical trial for early Alzheimer's disease.Alzheimer's research & therapy · 2025Trial
- MALDI-MSI-Guided Laser Capture Microdissection Coupled with MS for Integrated Spatial Multi-Omics in Mouse Brain.Life (Basel, Switzerland) · 2026Article
- Nicotinamide N-methyltransferase gene silencing is associated with upregulation of X-inactive specific transcript and downregulation of stemness-related transcription factors in ovarian cancer.Molecular biology reports · 2026Article
- Deficits of Alzheimer's Disease Neuropsychological Architecture Correlate with Specific Exosomal mRNA Expression: Evidence of a Continuum?International journal of molecular sciences · 2025Article
- Nicotinamide N-Methyltransferase in the Inflammatory Pathogenesis of Graves' Orbitopathy.Investigative ophthalmology & visual science · 2025Article
- Exploring NNMT: from metabolic pathways to therapeutic targets.Archives of pharmacal research · 2024Review
- Nicotinamide N-Methyltransferase (NNMT): A New Hope for Treating Aging and Age-Related Conditions.Metabolites · 2024Review
- Role of Epigenetic Modulation in Neurodegenerative Diseases: Implications of Phytochemical Interventions.Antioxidants (Basel, Switzerland) · 2024Review
- The Brain Metabolome Is Modified by Obesity in a Sex-Dependent Manner.International journal of molecular sciences · 2024Article
- The Role of NADPharmaceuticals (Basel, Switzerland) · 2024Review
- Molecular Mechanisms of IL18 in Disease.International journal of molecular sciences · 2023Review
- Nicotinamide N-methyltransferase and liver diseases.Genes & diseases · 2023Review
- Article
- Alpha-synucleinopathy reduces NMNAT3 protein levels and neurite formation that can be rescued by targeting the NAD+ pathway.Human molecular genetics · 2022Article
- Exploring Unconventional SAM Analogues To Build Cell-Potent Bisubstrate Inhibitors for Nicotinamide N-Methyltransferase.Angewandte Chemie (International ed. in English) · 2022Article
- Nicotinamide N-Methyltransferase: A Promising Biomarker and Target for Human Cancer Therapy.Frontiers in oncology · 2022Review
- Resilience in Long-Term Viral Infection: Genetic Determinants and Interactions.International journal of molecular sciences · 2021Article
- NicotinamideBiomolecules · 2021Review
- Potent Inhibition of NicotinamideJournal of medicinal chemistry · 2021Article
- Mechanisms and inhibitors of nicotinamideRSC medicinal chemistry · 2021Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have previously shown that the expression of nicotinamide N-methyltransferase (NNMT) is significantly increased in the brains of patients who have died of Parkinson's disease (PD). In this study, we have compared the expression of NNMT in post-mortem medial temporal lobe, hippocampus and cerebellum of 10 Alzheimer's disease (AD) and 9 non-disease control subjects using a combination of quantitative Western blotting, immunohistochemistry and dual-label confocal microscopy coupled with quantitative analysis of colocalisation. NNMT was detected as a single protein of 29 kDa in both AD and non-disease control brains, which was significantly increased in AD medial temporal lobe compared to non-disease controls (7.5-fold, P < 0.026). There was no significant difference in expression in the cerebellum (P = 0.91). NNMT expression in AD medial temporal lobe and hippocampus was present in cholinergic neurones with no glial localisation. Cell-type expression was identical in both non-disease control and AD tissues. These results are the first to show, in a proof-of-concept study using a small patient cohort, that NNMT protein expression is increased in the AD brain and is present in neurones which degenerate in AD. These results suggest that the elevation of NNMT may be a common feature of many neurodegenerative diseases. Confirmation of this overexpression using a larger AD patient cohort will drive the future development of NNMT-targetting therapeutics which may slow or stop the disease pathogenesis, in contrast to current therapies which solely address AD symptoms.
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