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Biomedicines
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Mechanistic Insights of Selective Autophagy in Neurodegenerative Diseases
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Mechanistic Insights of Selective Autophagy in Neurodegenerative Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 8063

Special Issue Editors

Dr. Ashok Iyaswamy

E-Mail Website
Guest Editor
Centre for Parkinson’s Disease Research, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong
Interests: autophagy lysosomal pathway (ALP); transcription factor EB, blood–brain barrier permeable drugs; biomaterials; autophagy inducers; animal models
Special Issues, Collections and Topics in MDPI journals
Dr. Chun Kit Benjamin Tong

E-Mail Website
Guest Editor
Centre for Parkinson’s Disease Research, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong
Interests: Alzheimer’s disease; calcium signaling pathways; high-throughput screening (HTS) of herbal drugs; neuropathophysiology
Dr. Sreenivasmurthy Sravan Gopalkrishnashetty

E-Mail Website
Guest Editor
Department of Neurology, University of Texas Medical Branch, Galveston, TX, USA
Interests: Alzheimer’s disease; Parkinson’s disease; autophagy; blood-brain permeable drug screening

Special Issue Information

Dear Colleagues,

Selectively targeting cytosolic components or organelles for degradation is a major surveillance mechanism employed in several cell types and animal models. Damaged organelles and protein aggregates are crucial hallmarks of several neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and so on. In this process, several selective autophagy receptors bind to the dysregulated cellular cargo via the Atg8/LC3/GABARAP proteins and promote their degradation. Modulating quality control mechanisms can alleviate the devastating effects of neurodegenerative diseases.

This Special Issue will focus on recent advances in selective autophagy in neurodegenerative diseases, aiming to foster an improved understanding of the roles of selective autophagy in the pathogenesis, propagation, and therapeutics of various neurodegenerative diseases.

We are inviting the submission of original research articles and reviews on, but not limited to: new findings on molecular key players, biomarkers, risk factors, molecular mechanisms, and therapeutic targets of neurodegenerative diseases.

Dr. Ashok Iyaswamy
Dr. Chun Kit Benjamin Tong
Dr. Sreenivasmurthy Sravan Gopalkrishnashetty
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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • Alzheimer’s disease
  • Parkinson’s disease
  • animal model
  • selective autophagy
  • autophagy-lysosomal pathway
  • small molecule
  • pathomechanisms
  • therapeutics
  • multiomics

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Published Papers (3 papers)

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Research

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21 pages, 7324 KiB  
Article
Aspartame Causes Developmental Defects and Teratogenicity in Zebra Fish Embryo: Role of Impaired SIRT1/FOXO3a Axis in Neuron Cells
by Athiram Pandaram, Jeyakumari Paul, Wankupar Wankhar, Abhimanyu Thakur, Sakshi Verma, Karthick Vasudevan, Dapkupar Wankhar, Ananth Kumar Kammala, Priyanshu Sharma, Ravindran Jaganathan, Ashok Iyaswamy and Ravindran Rajan
Biomedicines 2024, 12(4), 855; https://doi.org/10.3390/biomedicines12040855 - 12 Apr 2024
Cited by 4 | Viewed by 2088
Abstract
Aspartame, a widely used artificial sweetener, is present in many food products and beverages worldwide. It has been linked to potential neurotoxicity and developmental defects. However, its teratogenic effect on embryonic development and the underlying potential mechanisms need to be elucidated. We investigated [...] Read more.
Aspartame, a widely used artificial sweetener, is present in many food products and beverages worldwide. It has been linked to potential neurotoxicity and developmental defects. However, its teratogenic effect on embryonic development and the underlying potential mechanisms need to be elucidated. We investigated the concentration- and time-dependent effects of aspartame on zebrafish development and teratogenicity. We focused on the role of sirtuin 1 (SIRT1) and Forkhead-box transcription factor (FOXO), two proteins that play key roles in neurodevelopment. It was found that aspartame exposure reduced the formation of larvae and the development of cartilage in zebrafish. It also delayed post-fertilization development by altering the head length and locomotor behavior of zebrafish. RNA-sequencing-based DEG analysis showed that SIRT1 and FOXO3a are involved in neurodevelopment. In silico and in vitro analyses showed that aspartame could target and reduce the expression of SIRT1 and FOXO3a proteins in neuron cells. Additionally, aspartame triggered the reduction of autophagy flux by inhibiting the nuclear translocation of SIRT1 in neuronal cells. The findings suggest that aspartame can cause developmental defects and teratogenicity in zebrafish embryos and reduce autophagy by impairing the SIRT1/FOXO3a axis in neuron cells. Full article
(This article belongs to the Special Issue Mechanistic Insights of Selective Autophagy in Neurodegenerative Diseases)
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17 pages, 2984 KiB  
Article
Interaction of Tau with Kinesin-1: Effect of Kinesin-1 Heavy Chain Elimination on Autophagy-Mediated Mutant Tau Degradation
by Karthikeyan Selvarasu, Abhay Kumar Singh, Avinash Dakshinamoorthy, Sravan Gopalkrishnashetty Sreenivasmurthy, Ashok Iyaswamy, Moorthi Radhakrishnan, Supriti Patnaik, Jian-Dong Huang, Leonard L. Williams, Sanjib Senapati and Siva Sundara Kumar Durairajan
Biomedicines 2024, 12(1), 5; https://doi.org/10.3390/biomedicines12010005 - 19 Dec 2023
Cited by 3 | Viewed by 1901
Abstract
Natively unfolded tau has a low propensity to form aggregates, but in tauopathies, such as Alzheimer’s disease (AD), tau aggregates into paired helical filaments (PHFs) and neurofibrillary tangles (NFTs). Multiple intracellular transport pathways utilize kinesin-1, a plus-end-directed microtubule-based motor. Kinesin-1 is crucial in [...] Read more.
Natively unfolded tau has a low propensity to form aggregates, but in tauopathies, such as Alzheimer’s disease (AD), tau aggregates into paired helical filaments (PHFs) and neurofibrillary tangles (NFTs). Multiple intracellular transport pathways utilize kinesin-1, a plus-end-directed microtubule-based motor. Kinesin-1 is crucial in various neurodegenerative diseases as it transports multiple cargoes along the microtubules (MT). Kinesin-1 proteins cannot progress along MTs due to an accumulation of tau on their surfaces. Although kinesin-1-mediated neuronal transport dysfunction is well-documented in other neurodegenerative diseases, its role in AD has received less attention. Very recently, we have shown that knocking down and knocking out of kinesin-1 heavy chain (KIF5B KO) expression significantly reduced the level and stability of tau in cells and tau transgenic mice, respectively. Here, we report that tau interacts with the motor domain of KIF5B in vivo and in vitro, possibly through its microtubule-binding repeat domain. This interaction leads to the inhibition of the ATPase activity of the motor domain. In addition, the KIF5B KO results in autophagy initiation, which subsequently assists in tau degradation. The mechanisms behind KIF5B KO-mediated tau degradation seem to involve its interaction with tau, promoting the trafficking of tau through retrograde transport into autophagosomes for subsequent lysosomal degradation of tau. Our results suggest how KIF5B removal facilitates the movement of autophagosomes toward lysosomes for efficient tau degradation. This mechanism can be enabled through the downregulation of kinesin-1 or the disruption of the association between kinesin-1 and tau, particularly in cases when neurons perceive disturbances in intercellular axonal transport. Full article
(This article belongs to the Special Issue Mechanistic Insights of Selective Autophagy in Neurodegenerative Diseases)
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Review

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16 pages, 1226 KiB  
Review
Mechanistic Insights and Potential Therapeutic Approaches in PolyQ Diseases via Autophagy
by Mukul Jain, Nil Patil, Gholamreza Abdi, Maryam Abbasi Tarighat, Arifullah Mohammed, Muhammad Rajaei Ahmad Mohd Zain and Khang Wen Goh
Biomedicines 2023, 11(1), 162; https://doi.org/10.3390/biomedicines11010162 - 9 Jan 2023
Cited by 4 | Viewed by 3112
Abstract
Polyglutamine diseases are a group of congenital neurodegenerative diseases categorized with genomic abnormalities in the expansion of CAG triplet repeats in coding regions of specific disease-related genes. Protein aggregates are the toxic hallmark for polyQ diseases and initiate neuronal death. Autophagy is a [...] Read more.
Polyglutamine diseases are a group of congenital neurodegenerative diseases categorized with genomic abnormalities in the expansion of CAG triplet repeats in coding regions of specific disease-related genes. Protein aggregates are the toxic hallmark for polyQ diseases and initiate neuronal death. Autophagy is a catabolic process that aids in the removal of damaged organelles or toxic protein aggregates, a process required to maintain cellular homeostasis that has the potential to fight against neurodegenerative diseases, but this pathway gets affected under diseased conditions, as there is a direct impact on autophagy-related gene expression. The increase in the accumulation of autophagy vesicles reported in neurodegenerative diseases was due to an increase in autophagy or may have been due to a decrease in autophagy flux. These reports suggested that there is a contribution of autophagy in the pathology of diseases and regulation in the process of autophagy. It was demonstrated in various disease models of polyQ diseases that autophagy upregulation by using modulators can enhance the dissolution of toxic aggregates and delay disease progression. In this review, interaction of the autophagy pathway with polyQ diseases was analyzed, and a therapeutic approach with autophagy inducing drugs was established for disease pathogenesis. Full article
(This article belongs to the Special Issue Mechanistic Insights of Selective Autophagy in Neurodegenerative Diseases)
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