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Cross-Talk between Mitochondrial Dysfunction and Neuroinflammation in Central Nervous System Disorders

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 (31 October 2024) | Viewed by 3186

Special Issue Editor


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Guest Editor
Department of Cellular Signalling, Mossakowski Medical Research Centre Polish Academy of Sciences, Warsaw, Poland
Interests: neurodegeneration; neuroinflammation; mitochondria failure; autism spectrum disorders; synaptic plasticity; signal transduction; oxidative/nitrosative stress; alpha-synuclein
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Special Issue Information

Dear Colleagues,

Mitochondrial dysfunction and neuroinflammation have been linked to an array of brain disorders, from neurodevelopmental to neurodegenerative diseases such as autism spectrum disorders and Alzheimer’s and Parkinson’s disease, each characterized by distinct clinical manifestations and underlying pathological mechanisms. Both mitochondrial damage and the activation of neuroinflammatory pathways can mutually contribute to neuronal and synaptic dysfunction and thus to the progression of these apparently different diseases. On the one hand, mitochondria could be a pivotal element to the triggering of neuroinflammation through the release of damage-associated molecular patterns (DAMPs) that can stimulate various innate immune receptors to promote inflammation. On the other hand, the inflammatory factors released by activated glial cells might trigger specific signaling pathways which affect mitochondrial function. However, the cross-talk between mitochondrial dysfunction and neuroinflammatory activation is complex and not fully explained. Therefore, this Special Issue is designed to emphasize the link between mitochondrial dysfunction and neuroinflammation in different central nervous system (CNS) disorders. An in-depth understanding of the specific molecular mechanisms of mito-inflammation and the progression of neuroinflammation may contribute to the identification of new targets for the treatment of neuropsychiatric disorders. In this regard, we would like to encourage the submission of original papers providing new evidence on the connection between mitochondrial dysfunction and neuroinflammation in the etiology of brain disorders and review articles which address the above-mentioned topics.

Dr. Agata Adamczyk
Guest Editor

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Keywords

  • central nervous system
  • mitochondria
  • neuroinflammation
  • neurodegenerative diseases
  • neurodevelopmental disorders

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Published Papers (1 paper)

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Review

32 pages, 2349 KiB  
Review
SARS-CoV-2 Infection and Alpha-Synucleinopathies: Potential Links and Underlying Mechanisms
by Joanna Agata Motyl, Grażyna Gromadzka, Grzegorz Arkadiusz Czapski and Agata Adamczyk
Int. J. Mol. Sci. 2024, 25(22), 12079; https://doi.org/10.3390/ijms252212079 - 10 Nov 2024
Cited by 1 | Viewed by 2775
Abstract
Alpha-synuclein (α-syn) is a 140-amino-acid, intrinsically disordered, soluble protein that is abundantly present in the brain. It plays a crucial role in maintaining cellular structures and organelle functions, particularly in supporting synaptic plasticity and regulating neurotransmitter turnover. However, for reasons not yet fully [...] Read more.
Alpha-synuclein (α-syn) is a 140-amino-acid, intrinsically disordered, soluble protein that is abundantly present in the brain. It plays a crucial role in maintaining cellular structures and organelle functions, particularly in supporting synaptic plasticity and regulating neurotransmitter turnover. However, for reasons not yet fully understood, α-syn can lose its physiological role and begin to aggregate. This altered α-syn disrupts dopaminergic transmission and causes both presynaptic and postsynaptic dysfunction, ultimately leading to cell death. A group of neurodegenerative diseases known as α-synucleinopathies is characterized by the intracellular accumulation of α-syn deposits in specific neuronal and glial cells within certain brain regions. In addition to Parkinson’s disease (PD), these conditions include dementia with Lewy bodies (DLBs), multiple system atrophy (MSA), pure autonomic failure (PAF), and REM sleep behavior disorder (RBD). Given that these disorders are associated with α-syn-related neuroinflammation—and considering that SARS-CoV-2 infection has been shown to affect the nervous system, with COVID-19 patients experiencing neurological symptoms—it has been proposed that COVID-19 may contribute to neurodegeneration in PD and other α-synucleinopathies by promoting α-syn misfolding and aggregation. In this review, we focus on whether SARS-CoV-2 could act as an environmental trigger that facilitates the onset or progression of α-synucleinopathies. Specifically, we present new evidence on the potential role of SARS-CoV-2 in modulating α-syn function and discuss the causal relationship between SARS-CoV-2 infection and the development of parkinsonism-like symptoms. Full article
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