Autophagy in Neurological Disorders

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Neuroscience".

Deadline for manuscript submissions: 30 April 2026 | Viewed by 532

Special Issue Editors


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Guest Editor
Cancer Research UK Scotland Centre, Institute of Genetics and Cancer, The University of Edinburgh, Edinburgh, UK
Interests: autophagy; neurological disorders; cancer

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Guest Editor
Laboratory of Molecular Pathology, Department of Health Sciences, Università del Piemonte Orientale “A. Avogadro”, Via Solaroli 17, 28100 Novara, Italy
Interests: autophagy and protein metabolism in cancer and in neurodegeneration; epigenetics in cancer; nutraceuticals and probiotics in cancer and infectious diseases
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Special Issue Information

Dear Colleagues,

Autophagy is an intracellular lysosomal degradation pathway by which cytoplasmic cargoes are removed to maintain cellular homeostasis. Dysregulation of this process is linked to loss of cell proteostasis and linked to diverse pathologies. In this Special Issue, we aim to focus on the relevance of the autophagic process in maintaining neuronal health and how it is linked to neurological disorders. Autophagy is essential in neurons and glial cells that need to cope with prolonged and sustained operational stress, and thus autophagy is known to protect against different neurological disorders, such as neuroinfectious diseases, nerve injury diseases, and neurodegenerative diseases. To tackle these pathologies, it is crucial to understand the physiological relevance of autophagy in these cells and how this pathway is linked to pathologies in the nervous system. At the same time, this research remains critical to developing biomarkers and pharmacological agents. In this Special Issue, we welcome any publication related to autophagy, either general autophagy or selective autophagy, or general loss of cell proteostasis or lysosomal-related phenotypes in these disorders. Also, any studies linking autophagy to other neurodegenerative hallmarks, such as metabolism or oxidative stress, and any studies on the effect of targeting this pathway as a therapeutic approach.

Dr. Natalia Jimenez-Moreno
Prof. Dr. Ciro Isidoro
Guest Editors

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Keywords

  • autophagy
  • selective autophagy
  • neurodegeneration
  • proteostasis
  • lysosomes
  • aging
  • oxidative stress
  • aging
  • biomarkers
  • pharmacological agents

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Published Papers (1 paper)

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Research

20 pages, 2649 KB  
Article
Antiretroviral Drugs Impact Autophagy Differently in Primary Human Astrocytes
by Laura Cheney, Grace McDermott, Hillary Guzik and Joan W. Berman
Cells 2025, 14(23), 1904; https://doi.org/10.3390/cells14231904 - 1 Dec 2025
Viewed by 238
Abstract
While antiretroviral therapy (ART) has significantly improved the morbidity of HIV infection, ART may contribute to the pathogenesis of HIV associated neurocognitive impairment (HIV-NCI) by interfering with autophagic processes in astrocytes. Autophagy and mitophagy remove unwanted/damaged material and mitochondria from the intracellular environment, [...] Read more.
While antiretroviral therapy (ART) has significantly improved the morbidity of HIV infection, ART may contribute to the pathogenesis of HIV associated neurocognitive impairment (HIV-NCI) by interfering with autophagic processes in astrocytes. Autophagy and mitophagy remove unwanted/damaged material and mitochondria from the intracellular environment, respectively. Dysregulated autophagy in astrocytes, abundant CNS cells with crucial homeostatic functions, contributes to many neurodegenerative diseases. Few studies have examined effects of ART on autophagy in astrocytes. We treated primary human astrocytes with a common ART regimen and performed LC3B-II and p62 turnover assays. ART significantly inhibited both LC3B-II and p62 turnover. Since p62, one autophagy receptor that mediates mitophagy, autophagic clearance of mitochondria, turnover was inhibited, we also examined mitophagy. While ART decreased BNIP3L/Nix homodimers, there were no changes in PINK1, Parkin, Mt-CO2, mitochondrial mass, or mitochondria–lysosome colocalization, indicating that ART did not inhibit mitophagy. We show that antiretroviral drugs have distinct effects on autophagic processes in astrocytes, which represents an alteration in their homeostasis, a major function of autophagy. This likely contributes to HIV-NCI. Understanding these impacts is important for improving ART for PWH, who have, by necessity, ongoing ART exposure. It also facilitates development of therapies for HIV-NCI that may include modulation of autophagy. Full article
(This article belongs to the Special Issue Autophagy in Neurological Disorders)
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