Abstract
Parkinsons disease is a neurodegenerative movement disorder caused by a combination of environmental and genetic factors. Recent human genetic studies have identified five genes that are linked to Parkinsons disease (PD): α-synuclein, parkin, UCH-L1, DJ-1 and NR4A2. Among these genes, a variety of mutations in the human parkin locus have been found in many PD cases, both familial and sporadic. Parkin appears to be the most prevalent genetic factor in PD. It encodes for a protein-ubiquitin E3 ligase, whose loss-offunction mutations cause specific degeneration of dopamine (DA) neurons in substantia nigra in human patients. The accumulation of parkin substrates is thought to be the key factor in the selective death of DA neurons. Rapid progress in the identification of these substrates and the generation of genetic animal models has produced a plethora of knowledge about the biological function of parkin and its role in PD. These studies also offer novel pharmacological targets for the development of more selective therapeutic strategies. In this review, I will summarize results from this fast expanding field and discuss their potential implication in the treatment of Parkinsons disease.
Keywords: parkin, synuclein, parkinson's disease, ubiquitination, misfolding, microtubule, dopamine, tubulin
Current Neuropharmacology
Title: Genetic Factors in Parkinsons Disease and Potential Therapeutic Targets
Volume: 1 Issue: 4
Author(s): Jian Feng
Affiliation:
Keywords: parkin, synuclein, parkinson's disease, ubiquitination, misfolding, microtubule, dopamine, tubulin
Abstract: Parkinsons disease is a neurodegenerative movement disorder caused by a combination of environmental and genetic factors. Recent human genetic studies have identified five genes that are linked to Parkinsons disease (PD): α-synuclein, parkin, UCH-L1, DJ-1 and NR4A2. Among these genes, a variety of mutations in the human parkin locus have been found in many PD cases, both familial and sporadic. Parkin appears to be the most prevalent genetic factor in PD. It encodes for a protein-ubiquitin E3 ligase, whose loss-offunction mutations cause specific degeneration of dopamine (DA) neurons in substantia nigra in human patients. The accumulation of parkin substrates is thought to be the key factor in the selective death of DA neurons. Rapid progress in the identification of these substrates and the generation of genetic animal models has produced a plethora of knowledge about the biological function of parkin and its role in PD. These studies also offer novel pharmacological targets for the development of more selective therapeutic strategies. In this review, I will summarize results from this fast expanding field and discuss their potential implication in the treatment of Parkinsons disease.
Export Options
About this article
Cite this article as:
Feng Jian, Genetic Factors in Parkinsons Disease and Potential Therapeutic Targets, Current Neuropharmacology 2003; 1 (4) . https://dx.doi.org/10.2174/1570159033477053
DOI https://dx.doi.org/10.2174/1570159033477053 |
Print ISSN 1570-159X |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6190 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
- Announcements
- Forthcoming Thematic Issues
Related Articles
-
Editorial [Hot Topic:Neurobiology Wakes Up for Research on Sleep Disorders: An Integration of Basic and Clinical Research(Executive Editor: Luigi De Gennaro)]
Current Pharmaceutical Design Drug Therapy of Neuropathic Pain: Current Developments and Future Perspectives
Current Drug Targets Epidermolysis Bullosa: The Pediatricians Role
Current Pediatric Reviews Current & Future Therapies of Erectile Dysfunction in Neurological Disorders
Recent Patents on CNS Drug Discovery (Discontinued) Exogenous Hormonal Regulation in Breast Cancer Cells by Phytoestrogens and Endocrine Disruptors
Current Medicinal Chemistry Mobilization and Redistribution of Default Mode Network from Resting State to Task State in Amnestic Mild Cognitive Impairment
Current Alzheimer Research Pharmacological Therapy of Parkinson’s Disease: Current Options and New Avenues
Recent Patents on CNS Drug Discovery (Discontinued) Brain-gut Axis and Pentadecapeptide BPC 157: Theoretical and Practical Implications
Current Neuropharmacology Current Options and Perspectives in the Treatment of Diabetic Neuropathy
Current Pharmaceutical Design Familial Mutations and Post-translational Modifications of UCH-L1 in Parkinson's Disease and Neurodegenerative Disorders
Current Protein & Peptide Science Ezetimibe and Vascular Inflammation
Current Vascular Pharmacology Atypicality of Atypical Antipsychotics Revisited
Current Psychiatry Reviews Gene-Gene Interactions in a Context of Individual Variability in Antipsychotic Drug Pharmacogenomics
Current Pharmacogenomics and Personalized Medicine The Role of Blood-Brain Barrier Studies in the Pharmaceutical Industry
Current Drug Metabolism Ultra-micronized Palmitoylethanolamide: An Efficacious Adjuvant Therapy for Parkinson’s Disease
CNS & Neurological Disorders - Drug Targets Preparation, Physicochemical Evaluation and Characterization of Mucoadhesive Buccal Gels Impregnated with Benzydamine Hydrochloride for the Effective Treatment of Aphthous Stomatitis: Effect of Different Grades of HPMC Polymer on In vitro and Ex vivo Performance
Drug Delivery Letters New Technologies for the Diagnosis of Sleep Apnea
Current Hypertension Reviews Design of Cathepsin K Inhibitors for Osteoporosis
Current Topics in Medicinal Chemistry FDG PET/MR Imaging in Major Neurocognitive Disorders
Current Alzheimer Research Neuroprotective Gene Therapy for Parkinson’s Disease
Current Gene Therapy