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Molecular Advances in Neurodegenerative Diseases

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: closed (30 December 2024) | Viewed by 2896

Special Issue Editor

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases are extremely difficult to study for a number of reasons. First, animal models reproduce only some aspects of human disease. Second, the extremely long time course can obscure the events that initiate the process of degeneration. This implies that molecular changes seen later in the disease may be consequences and not causes of the degeneration. Third, it is difficult to make conclusive clinical diagnoses and separate clinical phenotypes, and so even powerful molecular techniques may not be successful.

The role of amyloid and tau in Alzheimer’s disease and the roles of alpha synuclein in Parkinson’s disease and TDP-43 in ALS and frontotemporal dementia are probably only the beginning of the molecular pathogenesis, and novel studies are critical.

Dr. Mark M. Stecker
Guest Editor

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Keywords

  • neurodegenerative diseases
  • Alzheimer’s disease
  • Parkinson’s disease
  • alpha synuclein
  • degeneration

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Published Papers (1 paper)

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Research

28 pages, 10113 KiB  
Article
Identification of a New Role of miR-199a-5p as Factor Implied in Neuronal Damage: Decreasing the Expression of Its Target X-Linked Anti-Apoptotic Protein (XIAP) After SCI
by Teresa Muñoz-Galdeano, David Reigada, Altea Soto, María Asunción Barreda-Manso, Pablo Ruíz-Amezcua, Manuel Nieto-Díaz and Rodrigo M. Maza
Int. J. Mol. Sci. 2024, 25(22), 12374; https://doi.org/10.3390/ijms252212374 - 18 Nov 2024
Viewed by 2643
Abstract
Spinal cord injury (SCI) results in a cascade of primary and secondary damage, with apoptosis being a prominent cause of neuronal cell death. The X-linked inhibitor of apoptosis (XIAP) plays a critical role in inhibiting apoptosis, but its expression is reduced following SCI, [...] Read more.
Spinal cord injury (SCI) results in a cascade of primary and secondary damage, with apoptosis being a prominent cause of neuronal cell death. The X-linked inhibitor of apoptosis (XIAP) plays a critical role in inhibiting apoptosis, but its expression is reduced following SCI, contributing to increased neuronal vulnerability. This study investigates the regulatory role of miR-199a-5p on XIAP expression in the context of SCI. Using bioinformatic tools, luciferase reporter assays, and in vitro and in vivo models of SCI, we identified miR-199a-5p as a post-transcriptional regulator of XIAP. Overexpression of miR-199a-5p significantly reduced XIAP protein levels, although no changes were observed at the mRNA level, suggesting translational repression. In vivo, miR-199a-5p expression was upregulated at 3 and 7 days post-injury, while XIAP expression inversely decreased in both neurons and oligodendrocytes, being particularly significant in the latter at 7 dpi. These findings suggest that miR-199a-5p contributes to the downregulation of XIAP and may exacerbate neuronal apoptosis after SCI. Targeting miR-199a-5p could offer a potential therapeutic strategy to modulate XIAP levels and reduce apoptotic cell death in SCI. Full article
(This article belongs to the Special Issue Molecular Advances in Neurodegenerative Diseases)
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