Neural Regeneration Research ›› 2026, Vol. 21 ›› Issue (3): 1130-1131.doi: 10.4103/NRR.NRR-D-24-01519

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Astrocyte glycolysis in Alzheimer’s disease: When the stars burn out

Simon M. Bell* , Heather Mortiboys   

  1. Sheffield Institute for Translational Neuroscience (SITraN), School of Medicine and Population Health, University of Sheffield, Sheffield, UK
  • Online:2026-03-15 Published:2025-07-04
  • Contact: Simon M. Bell, PhD, s.m.bell@sheffield.ac.uk.
  • Supported by:
    This work was funded by Wellcome 4ward North (Ref: 216340/Z/19/Z), ARUK Yorkshire Network Centre Small Grant Scheme, ARUK Preparatory Clinical Fellowship scheme (Ref: ARUKPCRF2016A-1), Academy of Medical Sciences Starter Grants for Clinical Lecturers Scheme (Ref: SGL028\1097), Parkinson’s UK (Ref: F1301), Michael J Fox Foundation (Ref: 005021), Australian Research Council (CE200100012), European Union Seventh Framework Programme (Ref: FP7/2007– 2013) under grant agreement no. 601055, and the NIHR Sheffield Biomedical Research Centre award (NIHR 203321) (to SMB). This is a summary of independent research carried out at the NIHR Sheffield Biomedical Research Centre (Translational Neuroscience). The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health and Social Care (DHSC).

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Abstract: Alzheimer’s disease (AD) is the most common form of dementia characterized pathologically by the deposition of amyloid plaques and hyperphosphorylated tau containing neurofibrillary tangles. The disease presents clinically with progressive memory loss and disruption of cognitive function. Currently, there is no cure for AD; recent advances in the therapeutics aimed at clearing the amyloid protein from the brain have led to potential disease stabilization, however, this does not prevent eventual disease progression (Cummings et al., 2024). The mechanisms that cause AD are complex and not fully understood. The main theories for disease development focus on the lack of clearance of amyloid or an increased accumulation of this protein. Changes to brain metabolism, genetic predispositions, inflammation, and the process of aging, all have roles in the establishment of the main sporadic form of the disease.