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Neurodegeneration: From Genetics to Molecules—2nd Edition

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: closed (28 August 2024) | Viewed by 993

Special Issue Editors


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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

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Guest Editor
Department of Medicine, University of Colorado-Anschutz Medical Campus, Aurora, CO 80045, USA
Interests: Alzheimer’s disease; neurodegenerative diseases

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
Dr. Subbiah Pugazhenthi
Guest Editors

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Keywords

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

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Published Papers (1 paper)

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Research

16 pages, 1393 KiB  
Article
Antinociceptive Behavior, Glutamine/Glutamate, and Neopterin in Early-Stage Streptozotocin-Induced Diabetic Neuropathy in Liraglutide-Treated Mice under a Standard or Enriched Environment
by Pavlina Gateva, Milen Hristov, Natasha Ivanova, Debora Vasileva, Alexandrina Ivanova, Zafer Sabit, Todor Bogdanov, Sonia Apostolova and Rumiana Tzoneva
Int. J. Mol. Sci. 2024, 25(19), 10786; https://doi.org/10.3390/ijms251910786 - 8 Oct 2024
Viewed by 432
Abstract
Diabetic neuropathy (DN) is a common complication of long-lasting type 1 and type 2 diabetes, with no curative treatment available. Here, we tested the effect of the incretin mimetic liraglutide in DN in mice with early-stage type 1 diabetes bred in a standard [...] Read more.
Diabetic neuropathy (DN) is a common complication of long-lasting type 1 and type 2 diabetes, with no curative treatment available. Here, we tested the effect of the incretin mimetic liraglutide in DN in mice with early-stage type 1 diabetes bred in a standard laboratory or enriched environment. With a single i.p. injection of streptozotocin 150 mg/kg, we induced murine diabetes. Liraglutide (0.4 mg/kg once daily, i.p. for ten days since the eighth post-streptozotocin day) failed to decrease the glycemia in the diabetic mice; however, it alleviated their antinociceptive behavior, as tested with formalin. The second phase of the formalin test had significantly lower results in liraglutide-treated mice reared in the enriched environment vs. liraglutide-treated mice under standard conditions [2.00 (0.00–11.00) vs. 29.00 (2.25–41.50) s, p = 0.016]. Liraglutide treatment, however, decreased the threshold of reactivity in the von Fray test. A significantly higher neopterin level was demonstrated in the diabetic control group compared to treatment-naïve controls and the liraglutide-treated diabetic mice (p < 0.001). The glutamine/glutamate ratio in both liraglutide-treated groups, either reared under standard conditions (p = 0.003) or an enriched environment (p = 0.002), was significantly higher than in the diabetic controls. This study demonstrates an early liraglutide effect on pain sensation in two streptozotocin-induced diabetes mouse models by reducing some inflammatory and oxidative stress parameters. Full article
(This article belongs to the Special Issue Neurodegeneration: From Genetics to Molecules—2nd Edition)
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