ijms-logo

Journal Browser

Journal Browser

Neurodegeneration: From Genetics to Molecules 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 28 August 2024 | Viewed by 394

Special Issue Editor


E-Mail Website
Guest Editor
Institute of Molecular Medicine, National Cheng Kung University, Tainan 70101, Taiwan
Interests: Alzheimer’s disease; WWOX; tumor suppressor; peptide drugs; cancer; cancer-induced neurodegeneration
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Molecular alterations play crucial roles in the pathogenesis of Alzheimer’s disease (AD) and other types of neurodegeneration. In 2019, the National Institute of Aging (NIA) announced that in addition to 20 known genes, there are five newly discovered genes, namely IQCK, ACE, ADAM10, ADAMTS1 and WWOX, which are associated with AD [1]. The functions of these five genes in the pathogenesis of AD and other neurodegeneration are largely unknown. Without a doubt, the addition of these new genes may assist our perspectives and understanding of the pathogenesis of AD and other neurodegeneration. For example, newborns with WWOX gene deficiency suffer severe neural diseases such as severe early infantile WWOX-related epileptic encephalopathy (WOREE) [2], metabolic disorder and early death. Furthermore, the downregulation of brain WWOX is frequently associated with AD progression in patients [3].

In this call for research and review papers, the specific topic will focus on the genetic alterations in proteins that contribute to the pathogenesis of AD and other neurodegeneration. We welcome articles related, but not limited to (1) gene-based molecular pathways in neurodegeneration; (2) gene-based therapy for neurodegeneration; (3) promising therapeutic strategies for neurodegeneration; (4) innate immunity in neurodegeneration, (5) proteins in chronic inflammation causing neurodegeneration in the brain; and (6) altered protein/protein interaction and signaling during signaling for inducing neurodegeneration. 

References: 

  1. Nat Genet. 201951, 414–430;
  2. Brain. 2021144, 3061–3077;
  3. Front Neurosci. 201812, 563.

Dr. Nan-Shan Chang
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

  • breast cancer
  • novel drugs
  • hormone receptor
  • inhibitor
  • immunotherapy
  • targeted agents

Published Papers

This special issue is now open for submission.
Back to TopTop