alexa
Reach Us +1-218-451-2974

GET THE APP

Novel Disease-modifying Drugs Inhibiting Alpha-synuclein Aggregation In Parkinson′s Disease Model Mice | 74775
ISSN: 2161-0460

Journal of Alzheimers Disease & Parkinsonism
Open Access

Like us on:

Our Group organises 3000+ Global Conferenceseries Events every year across USA, Europe & Asia with support from 1000 more scientific Societies and Publishes 700+ Open Access Journals which contains over 50000 eminent personalities, reputed scientists as editorial board members.

Open Access Journals gaining more Readers and Citations
700 Journals and 15,000,000 Readers Each Journal is getting 25,000+ Readers

This Readership is 10 times more when compared to other Subscription Journals (Source: Google Analytics)
Recommended Conferences
Google scholar citation report
Citations : 2275

Journal of Alzheimers Disease & Parkinsonism received 2275 citations as per google scholar report

Journal of Alzheimers Disease & Parkinsonism peer review process verified at publons
Indexed In
  • Index Copernicus
  • Google Scholar
  • Sherpa Romeo
  • Open J Gate
  • Genamics JournalSeek
  • Academic Keys
  • JournalTOCs
  • China National Knowledge Infrastructure (CNKI)
  • Electronic Journals Library
  • RefSeek
  • Hamdard University
  • EBSCO A-Z
  • OCLC- WorldCat
  • SWB online catalog
  • Virtual Library of Biology (vifabio)
  • Publons
  • Geneva Foundation for Medical Education and Research
  • Euro Pub
Share This Page

Novel disease-modifying drugs inhibiting alpha-synuclein aggregation in Parkinson′s disease model mice

3rd International Conference on Parkinsons disease and Movement Disorders

Kohji Fukunaga

Tohoku University, Japan

ScientificTracks Abstracts: J Alzheimers Dis Parkinsonism

DOI: 10.4172/2161-0460-C1-030

Abstract
Backgrounds: Accumulation and aggregation of alpha-synuclein in dopaminergic neurons is one of pathogenesis of Parkinson’s disease (PD), and its formation is partly regulated by long-chain polyunsaturated fatty acids (LCPUFAs) such as arachidonic acid (AA). Fatty acid binding protein 3 (FABP3, H-FABP) is critical for AA transport and metabolism in the brain. We recently demonstrated that FABP3 is highly expressed in dopaminergic neurons, especially in the substantia nigra pars compacta (SNpc). However, the pathophysiological relevance of FABP3 in PD remains unclear. Methods: Wild and FABP3 KO mice were treated with 1-methyl-1,2,3,6-tetrahydropiridine (MPTP) and investigated its neurotoxicity in the SNpc. Results: FABP3 KO mice were resistant to MPTP-induced dopaminergic neurodegeneration and motor deficits. Importatly, MPTP-induced alpha-synuclein accumulation in SNpc was attenuated in FABP3 KO mice compared with that in wild-type mice. In addition, we found that FABP3 overexpression promoted AA-induced alpha-synuclein oligomerization and induced cell death in PC12 cells. Over expression of FABP3 mutant protein lacking fatty-acid binding region did not promote AAinduced alpha-synuclein oligomerization and cell death. Finally, novel FABP3 ligands ameliorated MPTP-induced alphasynuclein accumulation/aggregation and rescued dopamine neurons from degeneration in MPTP-treated mice. Conclusion: Taken together, the formation of oligomers of alpha-synuclein is partly regulated by FABP3 through AA binding and metabolism in dopaminergic neurons, contributing to dopaminergic neuronal death seen in PD. We developed FABP ligands to develop as disease-modifying drugs for synucleinopathies in PD.
Biography

Kohji Fukunaga first discovered calcium/calmodulin-dependent protein kinase II (CaMKII) from brain in 1982. He received his PhD degrees from Kumamoto University School of Medicine in 1985. During 1988 to 1990, he worked as Research Fellow in Vanderbilt University (HHMI) under Professor TR Soderling. In 2002, he was appointed a Professor and Chairman in the faculty of graduate school of pharmaceutical sciences. He was Editor-in-Chief of Journal of Pharmacological Sciences (Elsevier) since 2012. He is interested in disease-modifying drug development for neurodegenerative disorders and psychiatry diseases such as autism and mental retardation.

Top