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Pathogenetic pathways in age-related neurodegenerations as novel therapeutic targets for Parkinson’s disease

Project description

Oxidative stress and ageing-related pathways as the targets to prevent Parkinson's disease

Parkinson's disease (PD) is the second most common neurodegenerative disorder and affects an estimated 1 % of the world's population over 60. The pathogenetic triggers of PD are mostly unknown, and current treatments only partially alleviate symptoms and do not restore normal neuronal function. The EU-funded PARNANT project will capitalise on the partners' expertise in C. elegans genetics and cell-based PD models to find the genetic pathways that mediate protection against neurodegeneration during oxidative stress and ageing. Previous studies identified 51 candidate genetic loci associated with age-related neurodegeneration in PD models and patients. Researchers aim to target these genes to alleviate the oxidative stress in the dopaminergic neurons and protect them against degeneration.

Objective

Parkinson’s disease (PD) is the second most common neurodegenerative disorder (after Alzheimer's) associated with oxidative stress and aging, and affects an estimated 1% of people worldwide over 60 years of age. The pathogenetic triggers of neurodegenerations are largely unknown. Current therapeutic interventions only partially alleviate symptoms and do not restore normal neuronal function or prevent progressive neurodegenerations. Identifying novel molecular targets and searching for therapeutic agents that block neurodegeneration and promote neuronal restoration is a key challenge in the field. I and the Host have together identified 51 candidate genetic loci associated with age-related neurodegenerations in PD model and PD patients, respectively. These candidate genes are evolutionarily conserved in both vertebrate and invertebrate animals. I hypothesize that some of these genes, via an evolutionarily conserved signal transduction pathway, alleviate the oxidative stress in the dopaminergic neurons and protect them against degeneration. This project combines my (C. elegans genetics) and Host (cell-based PD models) expertise to identify new genetic pathways that mediate protection against neurodegenerations during oxidative stress and aging. I expect that achieved goals of the proposal will be important discovery that should lead to novel therapeutic targeting for Parkinson’s disease, and other neurodegenerative proteinopathies. My long-term goal is to become an independent scientist and establish lab to find novel therapeutic targets and strategies for the diseases associated with oxidative stress, including PD. Gained research experience together with improving my teaching, mentoring and management skills during this fellowship will help me to achieve my goals and transition myself into independence.

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Funding Scheme

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MSCA-IF-EF-RI - RI – Reintegration panel

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Call for proposal

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(opens in new window) H2020-MSCA-IF-2018

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Coordinator

ACCADEMIA EUROPEA DI BOLZANO
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 183 473,28
Address
VIALE DRUSO 1
39100 Bolzano
Italy

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Region
Nord-Est Provincia Autonoma di Bolzano/Bozen Bolzano-Bozen
Activity type
Research Organisations
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Total cost

The total costs incurred by this organisation to participate in the project, including direct and indirect costs. This amount is a subset of the overall project budget.

€ 183 473,28
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