Molecular Mechanisms and Treatment of Parkinson’s Disease
A special issue of Neurology International (ISSN 2035-8377). This special issue belongs to the section "Movement Disorders and Neurodegenerative Diseases".
Deadline for manuscript submissions: 31 March 2026 | Viewed by 23
Special Issue Editor
Special Issue Information
Dear Colleagues,
Parkinson’s disease (PD) is a progressive neurodegenerative condition characterized by motor symptoms such as tremor, rigidity, bradykinesia, and postural instability and non-motor symptoms, such as cognitive dysfunction, sleep disturbances, and depression. The pathophysiological features of PD include a gradual loss of dopaminergic neurons in the substantia nigra pars compacta resulting in reduced dopamine in the striatum.
This Special Issue seeks to explore the complex mechanisms underlying the loss of dopaminergic neurons in PD such as mitochondrial damage, oxidative stress, neuroinflammation, protein misfolding and aggregation (p-tau, Aβ, and alpha-synuclein), and genetic mutations (SNCA, parkin, DJ-1, PINK1, LRRK2) driving these mechanisms. We welcome submissions that explore molecular mechanisms that explain mitochondrial damage and oxidative stress and papers that discuss glutamate mediated excitotoxicity as a contributor to oxidative stress. While several new treatments are being developed for PD, there is currently no treatment that can effectively slow disease progression. This topic will highlight newer treatments such as stem cell transplantation, gene therapies, therapies utilizing supplementation of neurotrophic factors, newer drug delivery systems, and non-pharmacological treatments such as aerobic exercise. This issue invites original research articles and reviews that are focused on translational science, and discusses how newer therapies can alleviate mitochondrial dysfunction in PD.
Dr. Anjali Sivaramakrishnan
Guest Editor
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Keywords
- Parkinson’s disease
- mitochondrial dysfunction
- oxidative stress
- neuroinflammation
- neuroprotection
- α-synuclein aggregation
- LRRK2/ PINK1
- mitochondria-targeted therapies
- stem cell transplantation
- gene therapy
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