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Abnormal Organelles and Protein Expression in Acute and Chronic Neurodegeneration
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Abnormal Organelles and Protein Expression in Acute and Chronic 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: 20 November 2025 | Viewed by 6088

Special Issue Editor

Prof. Dr. Francesco Fornai

E-Mail Website
Guest Editor
Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, 56124 Pisa, Italy
Interests: neuroanatomy; neuroscience; neurodegeneration; methamphetamine; autophagy; movement disorders; substances of abuse; morphology; ultrastructure
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In defining neurodegenerative disorders, we now include both slow chronic events which occur typically in Parkinson’s disease and degenerative dementia, as well as sudden acute neuronal loss, which recapitulates within a condensed time interval with most molecular events taking place in classic degenerative disorders, as demonstrated within ischemic penumbra following an ischemic stroke or prolonged epileptic discharges within epileptic penumbra. In keeping with such a wide definition of neurodegeneration, we should also include abnormal events which take place within neurons during reiterated exposure to drugs of abuse, which characterize neurodegeneration in the addicted brain. Similarly, psychiatric disorders such as bipolar disorders may feature degenerative phenomena.

In all conditions, a specific alteration to key organelles can often be described, and altered protein expression and protein clearance occur per se or related to the dysfunctional clearance organelles such as the autophagosomes, lysosomes, etc. The aim of this Special Issue is to gather evidence from various research field which share similar steps in producing a loss of neuronal integrity within specific brain areas ex vivo and in vivo, cell lines in vitro or protein conformation within in tubo systems. As such, the Special Issue focuses on collecting various findings from different research fields to represent a comprehensive overview of the pathways and subcellular components which characterize a variety of degenerative phenomena. Such a multi-faceted approach should attract scientists from different fields of neuroscience with expertise in various methods and topics.

Prof. Dr. Francesco Fornai
Guest Editor

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Keywords

  • brain ischemia
  • epileptic damage
  • basal ganglia pathology
  • catecholamine cell damage
  • excitotoxicity
  • autophagy
  • dopamine system norepinephrine system
  • protein unfolding
  • protein misfolding
  • cholinergic system

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Published Papers (3 papers)

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Research

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25 pages, 4438 KiB  
Article
Methamphetamine Increases Tubulo-Vesicular Areas While Dissipating Proteins from Vesicles Involved in Cell Clearance
by Gloria Lazzeri, Paola Lenzi, Carla L. Busceti, Stefano Puglisi-Allegra, Michela Ferrucci and Francesco Fornai
Int. J. Mol. Sci. 2024, 25(17), 9601; https://doi.org/10.3390/ijms25179601 - 4 Sep 2024
Viewed by 1073
Abstract
Cytopathology induced by methamphetamine (METH) is reminiscent of degenerative disorders such as Parkinson’s disease, and it is characterized by membrane organelles arranged in tubulo-vesicular structures. These areas, appearing as clusters of vesicles, have never been defined concerning the presence of specific organelles. Therefore, [...] Read more.
Cytopathology induced by methamphetamine (METH) is reminiscent of degenerative disorders such as Parkinson’s disease, and it is characterized by membrane organelles arranged in tubulo-vesicular structures. These areas, appearing as clusters of vesicles, have never been defined concerning the presence of specific organelles. Therefore, the present study aimed to identify the relative and absolute area of specific membrane-bound organelles following a moderate dose (100 µM) of METH administered to catecholamine-containing PC12 cells. Organelles and antigens were detected by immunofluorescence, and they were further quantified by plain electron microscopy and in situ stoichiometry. This analysis indicated an increase in autophagosomes and damaged mitochondria along with a decrease in lysosomes and healthy mitochondria. Following METH, a severe dissipation of hallmark proteins from their own vesicles was measured. In fact, the amounts of LC3 and p62 were reduced within autophagy vacuoles compared with the whole cytosol. Similarly, LAMP1 and Cathepsin-D within lysosomes were reduced. These findings suggest a loss of compartmentalization and confirm a decrease in the competence of cell clearing organelles during catecholamine degeneration. Such cell entropy is consistent with a loss of energy stores, which routinely govern appropriate subcellular compartmentalization. Full article
(This article belongs to the Special Issue Abnormal Organelles and Protein Expression in Acute and Chronic Neurodegeneration)
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18 pages, 4415 KiB  
Article
SARS-CoV-2 Nucleocapsid Protein Induces Tau Pathological Changes That Can Be Counteracted by SUMO2
by Franca Orsini, Marco Bosica, Annacarla Martucci, Massimiliano De Paola, Davide Comolli, Rosaria Pascente, Gianluigi Forloni, Paul E. Fraser, Ottavio Arancio and Luana Fioriti
Int. J. Mol. Sci. 2024, 25(13), 7169; https://doi.org/10.3390/ijms25137169 - 28 Jun 2024
Viewed by 2707
Abstract
Neurologic manifestations are an immediate consequence of SARS-CoV-2 infection, the etiologic agent of COVID-19, which, however, may also trigger long-term neurological effects. Notably, COVID-19 patients with neurological symptoms show elevated levels of biomarkers associated with brain injury, including Tau proteins linked to Alzheimer’s [...] Read more.
Neurologic manifestations are an immediate consequence of SARS-CoV-2 infection, the etiologic agent of COVID-19, which, however, may also trigger long-term neurological effects. Notably, COVID-19 patients with neurological symptoms show elevated levels of biomarkers associated with brain injury, including Tau proteins linked to Alzheimer’s pathology. Studies in brain organoids revealed that SARS-CoV-2 alters the phosphorylation and distribution of Tau in infected neurons, but the mechanisms are currently unknown. We hypothesize that these pathological changes are due to the recruitment of Tau into stress granules (SGs) operated by the nucleocapsid protein (NCAP) of SARS-CoV-2. To test this hypothesis, we investigated whether NCAP interacts with Tau and localizes to SGs in hippocampal neurons in vitro and in vivo. Mechanistically, we tested whether SUMOylation, a posttranslational modification of NCAP and Tau, modulates their distribution in SGs and their pathological interaction. We found that NCAP and Tau colocalize and physically interact. We also found that NCAP induces hyperphosphorylation of Tau and causes cognitive impairment in mice infected with NCAP in their hippocampus. Finally, we found that SUMOylation modulates NCAP SG formation in vitro and cognitive performance in infected mice. Our data demonstrate that NCAP induces Tau pathological changes both in vitro and in vivo. Moreover, we demonstrate that SUMO2 ameliorates NCAP-induced Tau pathology, highlighting the importance of the SUMOylation pathway as a target of intervention against neurotoxic insults, such as Tau oligomers and viral infection. Full article
(This article belongs to the Special Issue Abnormal Organelles and Protein Expression in Acute and Chronic Neurodegeneration)
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Review

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35 pages, 3838 KiB  
Review
Roles of the Receptor for Advanced Glycation End Products and Its Ligands in the Pathogenesis of Alzheimer’s Disease
by Wen Li, Qiuping Chen, Chengjie Peng, Dan Yang, Si Liu, Yanwen Lv, Langqi Jiang, Shijun Xu and Lihua Huang
Int. J. Mol. Sci. 2025, 26(1), 403; https://doi.org/10.3390/ijms26010403 - 5 Jan 2025
Cited by 1 | Viewed by 1800
Abstract
The Receptor for Advanced Glycation End Products (RAGE), part of the immunoglobulin superfamily, plays a significant role in various essential functions under both normal and pathological conditions, especially in the progression of Alzheimer’s disease (AD). RAGE engages with several damage-associated molecular patterns (DAMPs), [...] Read more.
The Receptor for Advanced Glycation End Products (RAGE), part of the immunoglobulin superfamily, plays a significant role in various essential functions under both normal and pathological conditions, especially in the progression of Alzheimer’s disease (AD). RAGE engages with several damage-associated molecular patterns (DAMPs), including advanced glycation end products (AGEs), beta-amyloid peptide (Aβ), high mobility group box 1 (HMGB1), and S100 calcium-binding proteins. This interaction impairs the brain’s ability to clear Aβ, resulting in increased Aβ accumulation, neuronal injury, and mitochondrial dysfunction. This further promotes inflammatory responses and oxidative stress, ultimately leading to a range of age-related diseases. Given RAGE’s significant role in AD, inhibitors that target RAGE and its ligands hold promise as new strategies for treating AD, offering new possibilities for alleviating and treating this serious neurodegenerative disease. This article reviews the various pathogenic mechanisms of AD and summarizes the literature on the interaction between RAGE and its ligands in various AD-related pathological processes, with a particular focus on the evidence and mechanisms by which RAGE interactions with AGEs, HMGB1, Aβ, and S100 proteins induce cognitive impairment in AD. Furthermore, the article discusses the principles of action of RAGE inhibitors and inhibitors targeting RAGE-ligand interactions, along with relevant clinical trials. Full article
(This article belongs to the Special Issue Abnormal Organelles and Protein Expression in Acute and Chronic Neurodegeneration)
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