The Role of Astrocytes in Neurodegenerative Diseases

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Cellular Biochemistry".

Deadline for manuscript submissions: 31 August 2025 | Viewed by 879

Special Issue Editor


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Guest Editor
Institute of Neuroanatomy, Uniklinik RWTH Aachen, Aachen, Germany
Interests: neurodegeneration; neuroinflammation; neuropharmacology; neuropsychology; neural stem cells
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Special Issue Information

Dear Colleagues,

Astrocytes, a prominent subtype of glial cells in the central nervous system, play crucial roles in metabolic support, structural integrity, and neuroprotection. They contribute significantly to maintaining homeostasis, clearing neurotransmitters, regulating the blood–brain barrier, and facilitating synaptic function. Dysfunctions in astrocytes and their transformation into reactive states due to pathological stimuli have been linked to the pathogenesis of various neurodegenerative disorders.

This Special Issue aims to highlight cutting-edge research on the involvement of astrocytes in the pathophysiology of neurodegenerative diseases. We invite submissions of original research articles, reviews, and communications that explore any aspect of astrocytic functions and dysfunctions in neurodegeneration.

Topics of interest include, but are not limited to, the following:

  • Molecular mechanisms underlying astrocyte–neuron interactions in neurodegenerative diseases;
  • The role of astrocytes in the clearance of misfolded proteins and neurotoxic molecules;
  • Astrocytic contributions to inflammation and neuroinflammatory responses;
  • Implications of astrocytic dysfunction in synaptic dysfunction and neuronal death;
  • Therapeutic strategies targeting astrocytes for neuroprotection and neuroregeneration.

Dr. Nima Sanadgol
Guest Editor

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Keywords

  • astrocytes
  • neurodegeneration
  • neuroinflammation
  • neuroprotection
  • neuroregeneration

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Published Papers (1 paper)

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Research

17 pages, 5883 KiB  
Article
Astrocytic Acid-Sensing Ion Channel 1a Contributes to the Development of Epileptic Cognitive Impairment
by Wen Li, Huimin Zhou, Xiaona Li, Gengyao Hu and Dong Wei
Biomolecules 2025, 15(1), 142; https://doi.org/10.3390/biom15010142 - 17 Jan 2025
Viewed by 550
Abstract
Reactive astrogliosis and acidosis, common features of epileptogenic lesions, express a high level of astrocytic acid-sensing ion channel-1a (ASIC1a), a proton-gated cation channel and key mediator of responses to neuronal injury. This study investigates the role of astrocytic ASIC1a in cognitive impairment following [...] Read more.
Reactive astrogliosis and acidosis, common features of epileptogenic lesions, express a high level of astrocytic acid-sensing ion channel-1a (ASIC1a), a proton-gated cation channel and key mediator of responses to neuronal injury. This study investigates the role of astrocytic ASIC1a in cognitive impairment following epilepsy. Status epilepticus (SE) in C57/BL6 mice was induced using lithium–pilocarpine; the impact of ASIC1a on astrocytes was assessed using rAAV–ASIC1a–NC and rAAV–ASIC1a–shRNA, injected in the CA3 region of mice. Behavioral assessments were conducted using the Morris water maze (MWM). Western blotting and immunofluorescence were applied to evaluate ASIC1a and Gfap expression while analyzing intracellular calcium and extracellular glutamate (Glu) concentrations in primary cultured astrocytes isolated from the brains of 1 to 3-day-old mice and treated LPS. Results showed enhanced astrocyte proliferation and ASIC1a expression in the dentate gyrus of epileptic mice 7, 21, and 28 days post-SE (all p < 0.05). Escape latency in the MWM further suggested that ASIC1a regulates cognitive function in mice with chronic epilepsy. LPS stimulation in vitro mimicked inflammatory responses, increasing ASIC1a after 24 h, which increased the concentration of intracellular calcium and extracellular expression of Glu; inhibition of ASIC1a expression reversed this process. To sum up, these data confirm that astrocytic ASIC1a may facilitate cognitive dysfunction post-epilepsy, presenting a potential therapeutic target. Full article
(This article belongs to the Special Issue The Role of Astrocytes in Neurodegenerative Diseases)
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