ArticleNeurobiology of disease2022
Alzheimer's disease is associated with disruption in thiamin transport physiology: A potential role for neuroinflammation.
Article in Neurobiology of disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Transaldolase 1 contributes to pentose phosphate pathway disruption and synaptic dysfunction in Alzheimer's disease.Translational neurodegeneration · 2026Article
- Unraveling Aberrant Metabolic Patterns in Alzheimer's Disease Subtypes: From Perturbed Metabolic Pathways to Candidate Drug Targets.Molecular neurobiology · 2026Article
- Mendelian Randomization Uncovers Potential Repurposable Medications for Neuropsychiatric Disorders.Current neuropharmacology · 2026Article
- Genome-wide association study identifies novel variants in olfactory, vitamin A, vitamin B, and cadherin pathways associated with learning and memory.Scientific reports · 2025Article
- Investigating the neuroprotective effects ofHeliyon · 2025Article
- Association between dietary vitamin B1 intake and cognitive function among older adults: a cross-sectional study.Journal of translational medicine · 2024Observational
- Identification of Novel Biomarkers for Alzheimer's Disease and Related Dementias Using Unbiased Plasma Proteomics.bioRxiv : the preprint server for biology · 2024Article
- Article
- Synthetic Thioesters of Thiamine: Promising Tools for Slowing Progression of Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- Revisiting the Role of Vitamins and Minerals in Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2023Review
- The biochemical basis of neurodegenerative disease: The role of immunoexcitoxicity and ways to possibly attenuate it.Surgical neurology international · 2023Review
- Pharmacological thiamine levels as a therapeutic approach in Alzheimer's disease.Frontiers in medicine · 2022Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is a neurodegenerative disease characterized by Amyloid-β peptide (Aβ) containing plaques and cognitive deficits. The pathophysiology of AD also involves neuroinflammation. Vitamin B1 (thiamin) is indispensable for normal cellular energy metabolism. Thiamin homeostasis is altered in AD, and its deficiency is known to aggravate AD pathology. Little, however, is known about possible alterations in level of expression of thiamin transporters-1 and -2 (THTR-1 and -2) in the brain of AD, and whether pro-inflammatory cytokines affect thiamin uptake by brain cells. We addressed these issues using brain tissue samples [prefrontal cortex (PFC) and hippocampus (HIP)] from AD patients and from 5XFAD mouse model of AD, together with cultured human neuroblastoma SH-SY5Y cells as model. Our results revealed a significantly lower expression of both THTR-1 and THTR-2 in the PFC and HIP of AD patients and 5XFAD mouse model of AD compared to appropriate normal controls. Further, we found that exposure of the SH-SY5Y cells to pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) led to a significant inhibition in thiamin uptake. Focusing on IL-1β, we found the inhibition in thiamin uptake to be time-dependent and reversible; it was also associated with a substantial reduction in expression of THTR-1 (but not THTR-2) protein and mRNA as well as a decrease in promoter activity of the SLC19A2 gene (which encodes THTR-1). Finally, using transcriptomic analysis, we found that thiamin availability in SH-SY5Y cells caused changes in the expression of genes relevant to AD pathways. These studies demonstrate, for the first time, that thiamin transport physiology/molecular biology parameters are negatively impacted in AD brain and that pro-inflammatory cytokines inhibit thiamin uptake by neuroblastoma cells. The results also support a possible role for thiamin in the pathophysiology of AD.
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