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Cells
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State-of-Art in Autophagy and Neurodegeneration
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State-of-Art in Autophagy and Neurodegeneration

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

Deadline for manuscript submissions: closed (25 July 2022) | Viewed by 15925

Special Issue Editors

Prof. Dr. Ciro Isidoro

E-Mail Website
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
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Tatiana Korolenko

E-Mail Website
Guest Editor
Scientific-Research Institute of Neurosciences and Medicine, Timakov Street 4, 630117 Novosibirsk, Russia
Interests: neurodegeneration; brain; autophagy inductors; overweight: liver; lysosomes; cysteine proteases and their inhibitors; lysosomotropic drugs

Special Issue Information

Dear Colleagues, 

Autophagy suppression was shown in several neurodegenerative diseases, like Alzheimer's, Parkinson's, and Huntington's diseases connected with the accumulation of amyloid-β, α-synuclein, and huntingtin, respectively.

Autophagy is also reduced in aging, which associates with physiological dementia, neuronal integrity loss and increased susceptibility to neurodegenerative disorders including Alzheimer's Disease, Parkinson Disease and Frontotemporal dementia, to name a few.

Thus, the autophagy activation through different pathways can reverse both neuronal dopaminergic and behavioral deficits in vivo and seems to be a promising therapy in pathology. Induction of autophagy as a means of improving the viability of cells and organisms is an attractive approach to experimental therapy of neurodegeneration.

This Special Issue of Cells will present research articles and reviews that cover the scope of autophagy and neurodegeneration. All scientists working in these fields are cordially invited to submit their manuscripts.

Prof. Dr. Ciro Isidoro
Prof. Dr. Tatyana A. Korolenko
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • autophagy
  • neurodegenerative diseases
  • neurodegeneration Parkinson’s disease,
  • Huntington’s disease
  • Alzheimer’s disease
  • mitophagy endosomal–lysosomal system
  • therapeutic
  • autophagy modulators

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

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20 pages, 6116 KB  
Article
Treatment with Autophagy Inducer Trehalose Alleviates Memory and Behavioral Impairments and Neuroinflammatory Brain Processes in db/db Mice
by Tatiana A. Korolenko, Nina I. Dubrovina, Marina V. Ovsyukova, Nataliya P. Bgatova, Michael V. Tenditnik, Alexander B. Pupyshev, Anna A. Akopyan, Natalya V. Goncharova, Chih-Li Lin, Evgeny L. Zavjalov, Maria A. Tikhonova and Tamara G. Amstislavskaya
Cells 2021, 10(10), 2557; https://doi.org/10.3390/cells10102557 - 27 Sep 2021
Cited by 23 | Viewed by 4578
Abstract
Autophagy attenuation has been found in neurodegenerative diseases, aging, diabetes mellitus, and atherosclerosis. In experimental models of neurodegenerative diseases, the correction of autophagy in the brain reverses neuronal and behavioral deficits and hence seems to be a promising therapy for neuropathologies. Our aim [...] Read more.
Autophagy attenuation has been found in neurodegenerative diseases, aging, diabetes mellitus, and atherosclerosis. In experimental models of neurodegenerative diseases, the correction of autophagy in the brain reverses neuronal and behavioral deficits and hence seems to be a promising therapy for neuropathologies. Our aim was to study the effect of an autophagy inducer, trehalose, on brain autophagy and behavior in a genetic model of diabetes with signs of neuronal damage (db/db mice). A 2% trehalose solution was administered as drinking water during 24 days of the experiment. Expressions of markers of autophagy (LC3-II), neuroinflammation (IBA1), redox state (NOS), and neuronal density (NeuN) in the brain were assessed by immunohistochemical analysis. For behavioral phenotyping, the open field, elevated plus-maze, tail suspension, pre-pulse inhibition, and passive avoidance tests were used. Trehalose caused a slight reduction in increased blood glucose concentration, considerable autophagy activation, and a decrease in the neuroinflammatory response in the brain along with improvements of exploration, locomotor activity, anxiety, depressive-like behavior, and fear learning and memory in db/db mice. Trehalose exerted some beneficial peripheral and systemic effects and partially reversed behavioral alterations in db/db mice. Thus, trehalose as an inducer of mTOR-independent autophagy is effective at alleviating neuronal and behavioral disturbances accompanying experimental diabetes. Full article
(This article belongs to the Special Issue State-of-Art in Autophagy and Neurodegeneration)
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Review

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40 pages, 30306 KB  
Review
Autophagy-Lysosomal Pathway as Potential Therapeutic Target in Parkinson’s Disease
by Srinivasa Reddy Bonam, Christine Tranchant and Sylviane Muller
Cells 2021, 10(12), 3547; https://doi.org/10.3390/cells10123547 - 15 Dec 2021
Cited by 40 | Viewed by 10030
Abstract
Cellular quality control systems have gained much attention in recent decades. Among these, autophagy is a natural self-preservation mechanism that continuously eliminates toxic cellular components and acts as an anti-ageing process. It is vital for cell survival and to preserve homeostasis. Several cell-type-dependent [...] Read more.
Cellular quality control systems have gained much attention in recent decades. Among these, autophagy is a natural self-preservation mechanism that continuously eliminates toxic cellular components and acts as an anti-ageing process. It is vital for cell survival and to preserve homeostasis. Several cell-type-dependent canonical or non-canonical autophagy pathways have been reported showing varying degrees of selectivity with regard to the substrates targeted. Here, we provide an updated review of the autophagy machinery and discuss the role of various forms of autophagy in neurodegenerative diseases, with a particular focus on Parkinson’s disease. We describe recent findings that have led to the proposal of therapeutic strategies targeting autophagy to alter the course of Parkinson’s disease progression. Full article
(This article belongs to the Special Issue State-of-Art in Autophagy and Neurodegeneration)
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