Neural Regeneration Research ›› 2026, Vol. 21 ›› Issue (10): 4908-4909.doi: 10.4103/NRR.NRR-D-25-01452

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Recognizing Alzheimer’s disease and Parkinson’s disease as astrogliopathies

Woojin Scott Kim*, Onur Tanglay, YuHong Fu*   

  1. Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia (Kim WS, Tanglay O, Fu YH)
    School of Medical Sciences, The University of Sydney, Sydney, NSW, Australia (Kim WS, TanglayO, Fu YH) 
    School of Biomedical Sciences, University of New South Wales, Sydney, NSW, Australia (Kim WS) 
    Randwick Clinical Campus, School of Clinical Medicine, Faculty of Medicine and Health, University of New South Wales, Randwick, NSW, Australia (Tanglay O)
  • Online:2026-10-15 Published:2026-06-13
  • Contact: YuHong Fu, MD, PhD, yuhong.fu@sydney.edu.au; Woojin Scott Kim, PhD, woojin.kim@sydney.edu.au.

Abstract: Astrocytes are the largest and most diverse glial cells in the central nervous system (CNS), with the main functions of providing support, nourishment and protection for neurons, the cells responsible for processing and transmitting information. Mounting evidence indicates that astrocytes are more than just support cells for neurons; they play complex and diverse roles that are essential for the homeostatic maintenance of the brain and spinal cord, with a key role as responders to pathological changes. As such, in recent years, there has been a dramatic increase in the interest of astrocytes in the pathogenesis of neurodegenerative diseases, Alzheimer’s disease (AD), and Parkinson’s disease (PD). Astrogliopathy is defined as pathological alterations in astrocytes, encompassing structural, molecular, or functional abnormalities that disrupt their normal roles in CNS homeostasis. These abnormalities include astrocyte reactivity, i.e. astrogliosis, degeneration, loss of supportive functions, metabolic dysregulation, impaired neurotransmitter clearance, disrupted blood-brain barrier interactions, and aberrant inflammatory signaling. Now, astrogliopathy is recognized to be a major player in both AD and PD pathogenesis. Understanding the relationship between astrocytic molecules and the accumulation of pathogenic proteins amyloid-β (Aβ) and α-synuclein will identify previously unrecognized pathways and targets, opening up new strategies for the therapeutic treatment of AD and PD, respectively.