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Molecular Mechanisms and Novel Therapeutic Approaches for Alzheimer’s Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 10 September 2024 | Viewed by 438

Special Issue Editor


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Guest Editor
Department of Clinical Chemistry and Biochemistry, Medical University of Lodz, 92-215 Lodz, Poland
Interests: polymers; restorative dentistry; bioactive dental materials; cell culture; apoptosis; cell signaling; western blot analysis; PCR; molecular cell biology; cancer biology; gene expression; electrophoresis; tissue culture

Special Issue Information

Dear Colleagues,

We are pleased to invite you to contribute to our Special Issue of the International Journal of Molecular Sciences (IJMS), entitled “Molecular Mechanisms and Novel Therapeutic Approaches for Alzheimer’s Disease”. This Special Issue will cover a selection of recent research topics and current review articles, reporting the latest updates on Alzheimer’s disease treatment. Alzheimer’s disease (AD) occurs as a result of neurodegenerative processes and it is characterized by the aggregation of misfolded and unfolded proteins among the neurons of the brain tissue, which is closely connected with a significant loss of neurons. Interestingly, it has been reported that AD pathogenesis and progression are strictly associated with common perturbation on the molecular level through the incorrect activation of selected molecular pathways. We welcome papers that address the molecular and cellular mechanisms underlying the pathogenesis of AD, molecular targets in AD, as well as novel therapeutic approaches for AD. This Special Issue is now open for submissions. If you are interested in contributing your work, please send a short abstract or tentative title to the Guest Editor or Editorial Office.

Dr. Wioletta Rozpędek-Kamińska
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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
  • dementia
  • amyloid-beta
  • amyloid aggregation
  • protein misfolding
  • Alzheimer’s disease signaling pathways
  • drug discovery
  • neuroprotection
  • Alzheimer’s disease treatment
  • neuroprotective strategies

Published Papers (1 paper)

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Research

11 pages, 3015 KiB  
Article
Involvement of Endolysosomes and Aurora Kinase A in the Regulation of Amyloid β Protein Levels in Neurons
by Zahra Afghah, Nabab Khan, Gaurav Datta, Peter W. Halcrow, Jonathan D. Geiger and Xuesong Chen
Int. J. Mol. Sci. 2024, 25(11), 6200; https://doi.org/10.3390/ijms25116200 - 4 Jun 2024
Viewed by 162
Abstract
Aurora kinase A (AURKA) is a serine/threonine-protein kinase that regulates microtubule organization during neuron migration and neurite formation. Decreased activity of AURKA was found in Alzheimer’s disease (AD) brain samples, but little is known about the role of AURKA in AD pathogenesis. Here, [...] Read more.
Aurora kinase A (AURKA) is a serine/threonine-protein kinase that regulates microtubule organization during neuron migration and neurite formation. Decreased activity of AURKA was found in Alzheimer’s disease (AD) brain samples, but little is known about the role of AURKA in AD pathogenesis. Here, we demonstrate that AURKA is expressed in primary cultured rat neurons, neurons from adult mouse brains, and neurons in postmortem human AD brains. AURKA phosphorylation, which positively correlates with its activity, is reduced in human AD brains. In SH-SY5Y cells, pharmacological activation of AURKA increased AURKA phosphorylation, acidified endolysosomes, decreased the activity of amyloid beta protein (Aβ) generating enzyme β-site amyloid precursor protein cleaving enzyme (BACE-1), increased the activity of the Aβ degrading enzyme cathepsin D, and decreased the intracellular and secreted levels of Aβ. Conversely, pharmacological inhibition of AURKA decreased AURKA phosphorylation, de-acidified endolysosomes, decreased the activity of cathepsin D, and increased intracellular and secreted levels of Aβ. Thus, reduced AURKA activity in AD may contribute to the development of intraneuronal accumulations of Aβ and extracellular amyloid plaque formation. Full article
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