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New Advances in Research on Alzheimer’s Disease: 2nd Edition

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: 31 December 2024 | Viewed by 1135

Special Issue Editors


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Guest Editor
IRCCS Mondino Fondation Genomic and Post Genomic Unit, 27100 Pavia, PV, Italy
Interests: coding and non coding RNA; gene expression; neurodegenerative diseases; genetic
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Alzheimer’s disease (AD) is considered the most common cause of dementia and is an incurable, progressive neurodegenerative disorder. To date, novel disease-modifying therapies have been shown to provide significant benefits to patients who suffer from this devastating disorder.

Moreover, preventive approaches of this pathology that are based on genetic predisposition, senolytic approaches, diet, or intellectual activity are increasingly relevant.

The aim of this Special Issue is to provide (but is not limited to) an overview of the recent advances in the field of novel therapy and targets for Alzheimer’s disease. In addition, data about preventive approaches are welcomed.

We invite researchers to submit original papers and reviews about the discovery of new targets and novel therapies for Alzheimer’s disease. Papers about other types of dementia will also be accepted.

Dr. Stella Gagliardi
Dr. Carlo Morasso
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. 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

  • therapy
  • prevention
  • new molecules
  • Alzheimer’s disease
  • genetics
  • nanoformulation
  • targets
  • dementia
  • biomarker discovery

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Published Papers (1 paper)

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8 pages, 229 KiB  
Perspective
Therapeutic Challenges Derived from the Interaction Among Apolipoprotein E, Cholesterol, and Amyloid in Alzheimer’s Disease
by Manuel Menendez-Gonzalez
Int. J. Mol. Sci. 2024, 25(22), 12029; https://doi.org/10.3390/ijms252212029 - 8 Nov 2024
Viewed by 867
Abstract
The isoform E4 of the Apolipoprotein E (ApoE) represents one of the strongest genetic risk factors for late-onset Alzheimer’s disease (AD). ApoE has key roles in cholesterol transport and amyloid-β (Aβ) metabolism, which are both central to AD pathogenesis. The E4 isoform has [...] Read more.
The isoform E4 of the Apolipoprotein E (ApoE) represents one of the strongest genetic risk factors for late-onset Alzheimer’s disease (AD). ApoE has key roles in cholesterol transport and amyloid-β (Aβ) metabolism, which are both central to AD pathogenesis. The E4 isoform has been implicated in reduced cholesterol homeostasis, increased Aβ aggregation, and heightened tau phosphorylation, contributing to amyloid plaques and neurodegeneration. This manuscript examines the complex interactions among ApoE isoforms, cholesterol metabolism, and amyloid pathology. Moreover, the therapeutic challenges associated with lipid-lowering agents (e.g., statins, PCSK9 inhibitors), anti-amyloid immunotherapies, and anticoagulants are described, focusing on ApoE4 carriers. Decision-making challenges are discussed by analyzing the pros and cons of these therapies. Full article
(This article belongs to the Special Issue New Advances in Research on Alzheimer’s Disease: 2nd Edition)
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