Molecular Mechanisms and Cellular Pathways in Parkinson's Disease
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".
Deadline for manuscript submissions: 31 March 2026 | Viewed by 3
Special Issue Editors
Interests: neurotoxicology; Parkinson's disease; exosomal mirnas; neurodegeneration; mitochondria; cell death and apoptosis
Interests: neurobiology of disease; neurodegeneration; neurotoxicology
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Parkinson’s disease (PD) is a debilitating neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the nigrostriatal pathway and the abnormal and toxic aggregation of α-synuclein. Disease progression is driven by mitochondrial dysfunction, impaired proteostasis, neuroinflammation, oxidative stress, and impaired synaptic function. The complex etiology of PD is linked to an interplay between genetic predisposition and environmental exposures, yet the precise molecular and cellular mechanisms remain elusive.
This Special Issue will showcase studies that advance our understanding of these pathways and how they are regulated under PD conditions. Topics of interest include molecular signaling cascades, cell-to-cell communication, neuroimmune responses, protein aggregation dynamics, and neuroprotective strategies. This Special Issue will also explore how environmental factors influence PD-related molecular mechanisms along with the genetic predisposition of the individual. Contributions should focus on unraveling the pathophysiology of PD, exploring the mechanisms driving neurodegeneration, and identifying potential targets to combat disease progression.
Dr. Fatema Currim
Prof. Dr. Jason Cannon
Guest Editors
Manuscript Submission Information
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Keywords
- Parkinson’s disease
- neurodegeneration
- mitochondrial dysfunction
- α-synuclein aggregation
- neurotoxicity
- neuroinflammation
- oxidative stress
- environmental factors
- gene–environment interactions
- cell death
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