You'll have to ask your competent? doctor to get those emerging therapeutic strategies aimed at modulating astrocyte function, so your astrocytes don't deteriorate.
Astrocytes in Brain Aging and Neurodegeneration: Cellular Mechanisms and Interventional Strategies
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Flávia C. A. Gomes | Isadora Matias
Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil
Correspondence: Flávia C. A. Gomes (fgomes@icb.ufrj.br)
Received: 5 November 2025 | Revised: 20 April 2026 | Accepted: 30 April 2026
Keywords: aging | astrocyte | glial cells | neurodegenerative diseases
ABSTRACT
Aging is characterized by progressive changes in the physiology of brain cells, which may contribute to cognitive decline,
ultimately leading to dementia and impaired quality of life. The increase in senescent cells, including glial cells in the brain,
is a general feature of normal aging and has been associated with age- related pathologies. Although recent evidence suggests
that astrocytes undergo senescence in these conditions, little is known about the molecular, and cellular mechanisms under
lying this event. This mini review, prepared as part of the special issue Neurochemistry in Latin America, provides a focused
overview of astrocyte dysfunction in physiological aging and neurodegenerative conditions, integrating findings from the field
alongside recent contributions from our group. We discuss how astrocyte aging contributes to cognitive decline and highlight
emerging evidence on how targeting astrocytes, both genetically and pharmacologically, may rescue cognitive decline associated with aging and neurodegenerative diseases. Astrocytes produce several molecules that control synapse formation and
function, which are decreased in the aging brain and in Alzheimer's disease models. In this context, recent studies indicate
that astrocytes undergo significant molecular and functional remodeling during aging. Notably, astrocyte senescence has
been associated with loss of lamin- B1, nuclear alterations, impaired synaptogenic and neuritogenic capacity, altered glutamate
metabolism, and mitochondrial dysfunction, all of which may contribute to reduced neuronal support and circuit integrity.
In parallel, recent advances have shown that astrocyte responses during aging also include diverse reactive states that vary
according to brain region, microenvironment, and disease stage. Importantly, senescence- associated and reactive features are
not mutually exclusive and may coexist or interact, further contributing to synaptic dysfunction and increased vulnerability
to neurodegeneration. Finally, we discuss emerging therapeutic strategies aimed at modulating astrocyte function, including targeting astrocyte- derived synaptogenic factors and metabolic pathways, as potential approaches to mitigate cognitive
decline. Together, current evidence indicates that astrocyte dysfunction in aging reflects a complex and dynamic spectrum
of cellular states that play a central role in brain vulnerability and represent promising targets for intervention in aging and
neurodegenerative diseases.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium,
provided the original work is properly cited.
© 2026 The Author(s). Journal of Neurochemistry published by John Wiley & Sons Ltd on behalf of International Society for
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