Guest Editors
Dr. Maria Gemma Nasoni
Email: maria.nasoni@uniurb.it
Affiliation: Department of Biomolecular Sciences, University of Urbino Carlo Bo, Urbino, Italy
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Research Interests: mitochondria, neuronal inflammation, melatonin, oxidative stress, ER stress
Summary
Neurodegenerative diseases are characterized by progressive neuronal loss and complex molecular dysfunctions, with mitochondrial dysfunction and neuroinflammation recognized as key drivers of disease onset and progression. Understanding the cellular and molecular mechanisms underlying these processes is critical for the development of effective therapeutic strategies. This Special Issue aims to provide a platform for original research and focused reviews that dissect the intricate interplay between mitochondrial impairment and neuroinflammatory pathways at the cellular level.
Key areas of focus include, but are not limited to:
· Melatonin-mediated neuroprotection: mitigating mitochondrial impairment and suppressing inflammatory pathways in the central nervous system.
· Molecular and cellular mechanisms linking mitochondrial dysfunction to neuronal cell death and synaptic deficits.
· Crosstalk between mitochondria, endoplasmic reticulum stress, and neuroinflammation in neurodegenerative disorders.
· Pharmacological or genetic interventions targeting mitochondrial dysfunction and/or neuroinflammatory signaling.
· Modulation of oxidative/nitrosative stress and downstream signaling pathways in neuronal cells.
· Novel cellular models and techniques for studying mitochondrial and inflammatory mechanisms in neurodegeneration.
By highlighting research that elucidates molecular mechanisms at the cellular level, this Special Issue seeks to advance our understanding of neurodegenerative diseases and inspire innovative therapeutic approaches. Authors are encouraged to submit studies that provide mechanistic insights, particularly those that establish causal links and regulatory pathways in neuronal and glial cells.
Keywords
mitochondrial dysfunction, neuroinflammation, neurodegenerative diseases, cellular mechanisms, melatonin, oxidative stress, ER stress, neuronal protection
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