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The role of oxidative stress on the degeneration of medullary respiratory neurons in an animal model of Parkinsons Disease

Grant number: 20/01831-7
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Effective date (Start): March 01, 2020
Effective date (End): April 30, 2021
Field of knowledge:Biological Sciences - Pharmacology - Biochemical and Molecular Pharmacology
Principal Investigator:Bárbara Falquetto
Grantee:Luiz Fernando de Araujo Trindade Pedrao
Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil
Associated research grant:19/00065-1 - Oxidative stress in respiratory control of Parkinson Disease animal model, AP.JP


Parkinsons Disease (PD) is a neurodegenerative and irreversible disease, characterized by loss of dopaminergic neurons in Substantia Nigra (SN). It consists of motor symptons, such as bradicinesia, postural instability, rigidity and reduction or absence of involuntary movements, and non-motor symptons, for example, problems in the respiratory tract caused by obstructuin of superior airways. It is known that many are the causes for dopaminergic neuron lesions in SN, from genetic factors to enviroment-individual factors. It is also a fact that the oxidative stress is directly linked to the neurodegeneration over Parkinsons Disease patients. Once the oxidative stress is also seen in medullary regions of control of breathing, notably in 6-hydroxidopamine (6-OHDA) models of PD, there is a highly loss in respiratory functions because of the degeneration of dopaminergic neurons, which can be due to increase of enzymatic activity of NADPH oxidase (NOX), responsible for the reduction of oxygen. This project aims to analyses the function of the NOX enzyme related to the oxidative stress and its relationship with the progressive loss of respiratory function, as a result of the degeneration of medullary respiratoru neurons and if treatment with apocynin, an unspecified inhibitor to that enzyme, can revert the respiratory deficit.

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