Respiratory anatomofunctional changes following apocinin treatment in a Parkinson's Disease model

• Grant number: 19/19810-9
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Effective date (Start): October 01, 2019
• Effective date (End): November 30, 2020
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: Bárbara Falquetto
• Grantee: Andre Luiz Ferreira do Nascimento
• 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

Abstract

As the second most common neurodegenerative disease affecting 2-3% of worldwide population above 65 years old, Parkinson's disease (PD) is characterized by motor and non-motor symptoms, including bradykinesia, rigidity, postural instability and respiratory deficits. The primary histological determinants of these symptoms are due to the death of neurons localized in the Substatia Nigra (SN), but little is known about what causes the initiation of this disease. Many studies point out to the direction that PD is caused by an increase of oxidative stress, and the NADPH family, main responsible for reactive oxygen species production, is responsible for this feature of the disease. The NOX family, the catalytic domain of NADPH oxidases includes many NOX homologous, and NOX2 is expressed in the medullary respiratory column. Due to these indicatives, the aim of this project is to investigate whether NADPH oxidase is involved in the respiratory group neurodegeneration, by NADPH oxidase inhibitor apocynin. For this, we will considerate the already known neurodegeneration of certain nuclei in the respiratory column in animal model of PD induced by 6-OHDA, where within the brainstem, there are groups of neurons that participate, modulate and integrate the respiratory functions, including Bötzinger, Pre-Bötzinger, rostral (rVRG) and caudal ventral respiratory group (cVRG) that showed reduced NK1 receptors imunoreactivity, and other clusters of neurons, such as retrotrapezoid nucleus (RTN) and nucleus of solitary tract (NTS) that showed reduction in phox2b expressing neurons. Altogether, is important to study the possible cause of the respiratory neurodegeneration and the role of the oxidative stress mediated by NADPH oxidase within these nuclei.