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Chemical Processes in Degenerative Diseases

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Chemical Biology".

Deadline for manuscript submissions: closed (31 July 2021) | Viewed by 3363

Special Issue Editor


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Guest Editor
Head of the Research Group "Cellular Adaptation and Bioenergetics", Institute for Molecular Medicine, Medical School Hamburg, Am Kaiserkai 1, 20457 Hamburg, Germany
Interests: cellular adaptation and metabolism; proteastasis; neuronal stress response; neuroprotection; aging

Special Issue Information

Dear Colleagues,

Aging and degenerative diseases are fundamentally characterized by an apparent increase in uncontrolled biochemical reactions. These spontaneous chemical processes comprise the undue aggregation and cross-linking of proteins as well as the opposite phenomenon: undue hydrolysis and fragmentation of essential macromolecular structures. Moreover, excessive oxidation frequently occurs in small molecules as well as proteins and other polymers to result in oxidative stress, although examples of uncontrolled reduction triggering cytotoxic cascades have also been described. Beyond these pairs of opposites, specific cases of isomerization, e.g., of amino acids, are notable markers of aging and degenerative disease. In many cases, however, it is yet uncertain whether disordering reactions indeed run faster during disease, or whether physiological repair processes have become slower.

The present Special Issue of Molecules entitled “Chemical Processes in Degenerative Diseases” is intended to highlight and summarize the current knowledge on these elementary chemical processes that are at the very heart of degenerative pathology. Common and uncommon chemical processes are equally suitable for this Special Issue. Analytical and interventional studies as well as review articles are welcome.

Prof. Dr. Parvana Hajieva
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 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. Molecules 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

  • aging
  • aggregation of macromolecules
  • cross-linking
  • hydrolysis
  • isomerization
  • fragmentation
  • oxidation
  • post-translational modification

Published Papers (1 paper)

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Research

23 pages, 6141 KiB  
Article
Palonosetron/Methyllycaconitine Deactivate Hippocampal Microglia 1, Inflammasome Assembly and Pyroptosis to Enhance Cognition in a Novel Model of Neuroinflammation
by Reem A. Mohamed, Dalaal M. Abdallah, Amany I. El-brairy, Kawkab A. Ahmed and Hanan S. El-Abhar
Molecules 2021, 26(16), 5068; https://0-doi-org.brum.beds.ac.uk/10.3390/molecules26165068 - 21 Aug 2021
Cited by 11 | Viewed by 2897
Abstract
Since westernized diet-induced insulin resistance is a risk factor in Alzheimer’s disease (AD) development, and lipopolysaccharide (LPS) coexists with amyloid β (Aβ)1-42 in these patients, our AD novel model was developed to resemble sporadic AD by injecting LPS into high fat/fructose diet (HFFD)-fed [...] Read more.
Since westernized diet-induced insulin resistance is a risk factor in Alzheimer’s disease (AD) development, and lipopolysaccharide (LPS) coexists with amyloid β (Aβ)1-42 in these patients, our AD novel model was developed to resemble sporadic AD by injecting LPS into high fat/fructose diet (HFFD)-fed rats. The neuroprotective potential of palonosetron and/or methyllycaconitine, 5-HT3 receptor and α7 nAChR blockers, respectively, was evaluated after 8 days of daily administration in HFFD/LPS rats. All regimens improved histopathological findings and enhanced spatial memory (Morris Water Maze); however, palonosetron alone or with methyllycaconitine promoted animal performance during novel object recognition tests. In the hippocampus, all regimens reduced the expression of glial fibrillary acidic protein and skewed microglia M1 to M2 phenotype, indicated by the decreased M1 markers and the enhanced M2 related parameters. Additionally, palonosetron and its combination regimen downregulated the expression of ASC/TMS1, as well as levels of inflammasome downstream molecules and abated cleaved caspase-1, interleukin (IL)-1β, IL-18 and caspase-11. Furthermore, ACh and 5-HT were augmented after being hampered by the insult. Our study speculates that blocking 5-HT3 receptor using palonosetron overrides methyllycaconitine to combat AD-induced neuroinflammation and inflammasome cascade, as well as to restore microglial function in a HFFD/LPS novel model for sporadic AD. Full article
(This article belongs to the Special Issue Chemical Processes in Degenerative Diseases)
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