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Unraveling the Molecular Mechanisms of Neurodegeneration
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Unraveling the Molecular Mechanisms of Neurodegeneration

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: 28 February 2025 | Viewed by 1341

Special Issue Editor

Dr. Michela Ferrucci

E-Mail Website
Guest Editor
Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, 56126 Pisa, Italy
Interests: neurodegeneration; spinal cord; motor neurons; glioblastoma; autophagy; light microscopy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases are among the leading causes of disability and death worldwide, primarily due to their impact on motor and cognitive functions. The incidence of these disorders, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis, is on the rise, mainly due to the aging population.

A variety of genetic and environmental factors have been identified as contributors to the pathogenesis of these diseases. Despite their distinct pathological mechanisms, neurodegenerative diseases share several common features, such as mitochondrial dysfunction, oxidative stress, aberrant exon splicing, and accumulation of misfolded/pathological proteins. Understanding these shared mechanisms that lead to the progressive loss of neurons remains one of the most significant challenges for neuroscientists today.

This Special Issue will collect scientific contributions that may enhance our understanding of established mechanisms or propose novel pathways involved in neuronal death. These insights will not only deepen our understanding of neurodegeneration but also provide new directions for developing future therapies to combat these devastating conditions.

Dr. Michela Ferrucci
Guest Editor

Manuscript Submission Information

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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

  • protein accumulation
  • mitochondria
  • genetic and epigenetic alterations
  • oxidative stress
  • apoptosis
  • autophagy

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Published Papers (2 papers)

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Research

14 pages, 3694 KiB  
Article
Light-Sheet Fluorescence Imaging Reveals Three-Dimensional Amyloid Burden Reduction Following Five Weeks of Swimming Exercise in Alzheimer’s Mouse
by Hye Joo Son and Suk Hyun Lee
Int. J. Mol. Sci. 2025, 26(3), 1249; https://doi.org/10.3390/ijms26031249 - 31 Jan 2025
Viewed by 264
Abstract
Emerging evidence from observational studies suggests that lifestyle modifications, particularly moderate-intensity exercise, may confer neuroprotective benefits against dementia, potentially by enhancing brain resistance through clearance mechanisms. Using light-sheet fluorescence microscopy (LSFM) with tissue clearing, we investigated the role of voluntary swimming in ameliorating [...] Read more.
Emerging evidence from observational studies suggests that lifestyle modifications, particularly moderate-intensity exercise, may confer neuroprotective benefits against dementia, potentially by enhancing brain resistance through clearance mechanisms. Using light-sheet fluorescence microscopy (LSFM) with tissue clearing, we investigated the role of voluntary swimming in ameliorating β-amyloid pathology in a transgenic Alzheimer’s disease (AD) mouse model. Twenty 52-week-old hAPPsw mice were randomly divided into a 5-week voluntary swimming intervention group and a control group (each n = 10). Each session included a 10-min swim followed by a 10-min rest, escalating from one session per day in the first week to three sessions per day by the fifth week. The excised brains were prepared using tissue-clearing and volume immunostaining with thioflavin-S for β-amyloid. For LSFM imaging, the individual plaque area and volume, total plaque load, and morphological parameters were quantified via an Imaris-based three-dimensional (3D) volumetric surface model. Visual comparison revealed that the intervention group presented significantly lower β-amyloid accumulation. The total surface volume of β-amyloid accumulation in the intervention group was significantly lower than that of the control group (intervention, 122,180,948 μm3 [105,854,660–169,063,081]; control, 167,201,016 μm3 [139,367,765–193,535,450]; p = 0.043). There were no significant differences in the morphological parameters, such as ellipticity and sphericity. Our LSFM study demonstrated notable reductions in β-amyloid, as evidenced by a decrease in total surface volume, in 52-week-old transgenic mice after a 5-week structured swimming program, supporting the notion that even in advanced AD stages, leisure-time voluntary swimming serves as an efficacious intervention for augmenting resistance to pathology. Full article
(This article belongs to the Special Issue Unraveling the Molecular Mechanisms of Neurodegeneration)
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16 pages, 2521 KiB  
Article
A Reduction in Mitophagy Is Associated with Glaucomatous Neurodegeneration in Rodent Models of Glaucoma
by Renuka M. Chaphalkar, Bindu Kodati, Prabhavathi Maddineni, Shaoqing He, Calvin D. Brooks, Dorota L. Stankowska, Shaohua Yang, Gulab Zode and Raghu R. Krishnamoorthy
Int. J. Mol. Sci. 2024, 25(23), 13040; https://doi.org/10.3390/ijms252313040 - 4 Dec 2024
Viewed by 793
Abstract
Glaucoma is a heterogenous group of optic neuropathies characterized by the degeneration of optic nerve axons and the progressive loss of retinal ganglion cells (RGCs), which could ultimately lead to vision loss. Elevated intraocular pressure (IOP) is a major risk factor in the [...] Read more.
Glaucoma is a heterogenous group of optic neuropathies characterized by the degeneration of optic nerve axons and the progressive loss of retinal ganglion cells (RGCs), which could ultimately lead to vision loss. Elevated intraocular pressure (IOP) is a major risk factor in the development of glaucoma, and reducing IOP remains the main therapeutic strategy. Endothelin-1 (ET-1), a potent vasoactive peptide, has been shown to produce neurodegenerative effects in animal models of glaucoma. However, the detailed mechanisms underlying ET-1-mediated neurodegeneration in glaucoma are not completely understood. In the current study, using a Seahorse Mitostress assay, we report that ET-1 treatment for 4 h and 24 h time points causes a significant decline in various parameters of mitochondrial function, including ATP production, maximal respiration, and spare respiratory capacity in cultured RGCs. This compromise in mitochondrial function could trigger activation of mitophagy as a quality control mechanism to restore RGC health. Contrary to our expectation, we observed a decrease in mitophagy following ET-1 treatment for 24 h in cultured RGCs. Using Morrison’s model of ocular hypertension in rats, we investigated here, for the first time, changes in mitophagosome formation by analyzing the co-localization of LC-3B and TOM20 in RGCs. We also injected ET-1 (24 h) into transgenic GFP-LC3 mice to analyze the formation of mitophagosomes in vivo. In Morrison’s model of ocular hypertension, as well as in ET-1 injected GFP-LC3 mice, we found a decrease in co-localization of LC3 and TOM20, indicating reduced mitophagy. Taken together, these results demonstrate that both ocular hypertension and ET-1 administration in rats and mice lead to reduced mitophagy, thus predisposing RGCs to neurodegeneration. Full article
(This article belongs to the Special Issue Unraveling the Molecular Mechanisms of Neurodegeneration)
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