Starved synapses: Gut microbiome dysbiosis and its role in Alzheimer's glucose impairment.
R, U., S, S., R, M., PS, K., S, V., & M, S. (2026). Starved synapses: Gut microbiome dysbiosis and its role in Alzheimer's glucose impairment.. International review of neurobiology. https://doi.org/10.1016/bs.irn.2026.01.010
R U, S S, R M, PS K, S V, M S. Starved synapses: Gut microbiome dysbiosis and its role in Alzheimer's glucose impairment.. International review of neurobiology. 2026; doi: 10.1016/bs.irn.2026.01.010
R U, S S, R M, et al. Starved synapses: Gut microbiome dysbiosis and its role in Alzheimer's glucose impairment.[J]. International review of neurobiology. 2026. DOI: 10.1016/bs.irn.2026.01.010.
@article{r2026,
author = {Upadhyay R and Santhosh S and Malathi R and Kumari PS and Vijayanand S and Sevanan M},
title = {Starved synapses: Gut microbiome dysbiosis and its role in Alzheimer's glucose impairment.},
journal = {International review of neurobiology},
year = {2026},
doi = {10.1016/bs.irn.2026.01.010},
note = {PMID: 42276619},
}
TY - JOUR AU - Upadhyay R AU - Santhosh S AU - Malathi R AU - Kumari PS AU - Vijayanand S AU - Sevanan M TI - Starved synapses: Gut microbiome dysbiosis and its role in Alzheimer's glucose impairment. T2 - International review of neurobiology PY - 2026 DO - 10.1016/bs.irn.2026.01.010 AN - PMID:42276619 ER -
Alzheimer's disease (AD) is increasingly recognised as a multifactorial disorder driven by metabolic, microbial, and neuroinflammatory imbalances. The study of the research results proposes that gut dysbiosis and impaired brain glucose metabolism are closely interrelated through the gut-brain metabolism axis. Changes in the intestinal microbiome may disrupt insulin sensitivity, cause systemic inflammation, and disrupt the blood-brain barrier, worsening neuronal glucose deficits and facilitating amyloid-β (Aβ) aggregation and tau phosphorylation. Alongside, neurodegenerative cascades are further enhanced by neuronal metabolic reprogramming, characterised by decreased glucose uptake, dysfunctional glycolytic enzymes, and oxidative stress. Short-chain fatty acids (SCFAs) are mainly butyrate, which have a neuroprotective effect in regulating inflammation and gut integrity, and dysbiosis causes increased pro-inflammatory cytokines and endotoxin leakage. This two-way communication network provides new therapeutic opportunities, such as probiotics, prebiotics, nutritional control, and metabolic reprogramming interventions, to regain homeostasis and prevent the advancement of AD.