Understanding the Interplay Between Autophagy and Neurodegeneration

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

Deadline for manuscript submissions: 10 May 2025 | Viewed by 1728

Special Issue Editors


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Guest Editor
Unidad Asociada Neurodeath, Universidad de Castilla-La Mancha, 02006 Albacete, Spain
Interests: autophagy; pharmacology; neurodegenerative diseases
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Unidad Asociada Neurodeath, Universidad de Castilla-La Mancha, 02006 Albacete, Spain
Interests: neurodegeneration; pharmacology; inflammation; cancer

Special Issue Information

Dear Colleagues,

Autophagy (or macroautophagy) is one of the most important cellular mechanisms involved in the maintenance of homeostasis in the Central Nervous System. It is characterized by the formation of well-known double-membrane vesicles or autophagosomes, which trap dysfunctional organelles and intracellular material potentially dangerous for neural cells, such as misfolded proteins, and deliver them to lysosomes for enzymatic degradation. This catabolic process is essential to avoid the accumulation of toxic content in neurons, and it is tightly controlled by key proteins such as mTOR, Ulk1, Beclin-1 and several ATG proteins. Although autophagic activity is induced in response to stressful situations to mitigate neuronal damage, long-term dysregulation of this pathway, by upregulation or downregulation, has emerged as a relevant cause of neurodegeneration, which contributes to the progression of many neurodegenerative diseases, such as Parkinson´s disease or Alzheimer disease. This Special Issue welcomes experts in the field to submit original research articles and reviews focused on studying the relationship between autophagy and neurodegeneration, including how autophagy imbalance aggravates neuronal survival and contributes to neurodegenerative diseases, as well as how new therapeutic alternatives could reduce neurodegeneration through autophagy modulation.

Dr. María Dolores Pérez-Carrión
Prof. Dr. Inmaculada Posadas
Guest Editors

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Keywords

  • autophagy
  • neurodegeneration
  • ATG
  • protein aggregates
  • misfolded proteins
  • toxic stimuli

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Published Papers (1 paper)

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Review

21 pages, 1753 KiB  
Review
V-ATPase Dysfunction in the Brain: Genetic Insights and Therapeutic Opportunities
by Antonio Falace, Greta Volpedo, Marcello Scala, Federico Zara, Pasquale Striano and Anna Fassio
Cells 2024, 13(17), 1441; https://doi.org/10.3390/cells13171441 - 28 Aug 2024
Viewed by 1454
Abstract
Vacuolar-type ATPase (v-ATPase) is a multimeric protein complex that regulates H+ transport across membranes and intra-cellular organelle acidification. Catabolic processes, such as endocytic degradation and autophagy, strictly rely on v-ATPase-dependent luminal acidification in lysosomes. The v-ATPase complex is expressed at high levels [...] Read more.
Vacuolar-type ATPase (v-ATPase) is a multimeric protein complex that regulates H+ transport across membranes and intra-cellular organelle acidification. Catabolic processes, such as endocytic degradation and autophagy, strictly rely on v-ATPase-dependent luminal acidification in lysosomes. The v-ATPase complex is expressed at high levels in the brain and its impairment triggers neuronal dysfunction and neurodegeneration. Due to their post-mitotic nature and highly specialized function and morphology, neurons display a unique vulnerability to lysosomal dyshomeostasis. Alterations in genes encoding subunits composing v-ATPase or v-ATPase-related proteins impair brain development and synaptic function in animal models and underlie genetic diseases in humans, such as encephalopathies, epilepsy, as well as neurodevelopmental, and degenerative disorders. This review presents the genetic and functional evidence linking v-ATPase subunits and accessory proteins to various brain disorders, from early-onset developmental epileptic encephalopathy to neurodegenerative diseases. We highlight the latest emerging therapeutic strategies aimed at mitigating lysosomal defects associated with v-ATPase dysfunction. Full article
(This article belongs to the Special Issue Understanding the Interplay Between Autophagy and Neurodegeneration)
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