Special Issue "Brain Metabolomics: New Perspective on Neurodegenerative Disorders"

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Pharmacology and Drug Metabolism".

Deadline for manuscript submissions: 30 June 2022.

Special Issue Editor

Dr. Charbel Moussa
E-Mail Website
Guest Editor
Department of Neurology, Georgetown University Medical Center, Washington, DC, USA
Interests: neurodegenerative diseases, PD, AD, ALS, LBD, etc.; blood brain barrier and angiogenesis; autopahgy; drug development

Special Issue Information

Dear colleagues,

This Special Issues broadly discusses protein clearance mechanisms via autophagy, the proteasome, and the lysosome in neurodegenerative diseases. It also will consider the direct effects on angiogenesis and the blood–brain barrier in health, disease and response to treatments. Inflammatory processes that are concurrent or independent of neurotoxic protein accumulation will also be considered. Papers concerning drug development as a strategy to treat neurodegeneration via manipulation of autophagy, the lysosome, and inflammation and restoration of the blood–brain barrier are particularly welcome.

Dr. Charbel Moussa
Guest Editor

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 papers will be 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. Metabolites 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 1800 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
  • angiogenesis
  • new drug
  • drug developments
  • neuroinflammation
  • Alpha-synuclein
  • Tau
  • amyloid
  • TDP_43

Published Papers (1 paper)

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Research

Article
Novel Ubiquitin Specific Protease-13 Inhibitors Alleviate Neurodegenerative Pathology
Metabolites 2021, 11(9), 622; https://doi.org/10.3390/metabo11090622 (registering DOI) - 15 Sep 2021
Viewed by 806
Abstract
Ubiquitin Specific Protease-13 (USP13) promotes protein de-ubiquitination and is poorly understood in neurodegeneration. USP13 is upregulated in Alzheimer’s disease (AD) and Parkinson’s disease (PD), and USP13 knockdown via shRNA reduces neurotoxic proteins and increases proteasome activity in models of neurodegeneration. We synthesized novel [...] Read more.
Ubiquitin Specific Protease-13 (USP13) promotes protein de-ubiquitination and is poorly understood in neurodegeneration. USP13 is upregulated in Alzheimer’s disease (AD) and Parkinson’s disease (PD), and USP13 knockdown via shRNA reduces neurotoxic proteins and increases proteasome activity in models of neurodegeneration. We synthesized novel analogues of spautin-1 which is a non-specific USP13 inhibitor but unable to penetrate the brain. Our synthesized small molecule compounds are able to enter the brain, more potently inhibit USP13, and significantly reduce alpha-synuclein levels in vivo and in vitro. USP13 inhibition in transgenic mutant alpha-synuclein (A53T) mice increased the ubiquitination of alpha-synuclein and reduced its protein levels. The data suggest that novel USP13 inhibitors improve neurodegenerative pathology via antagonism of de-ubiquitination, thus alleviating neurotoxic protein burden in neurodegenerative diseases. Full article
(This article belongs to the Special Issue Brain Metabolomics: New Perspective on Neurodegenerative Disorders)
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