| Grant number: | 21/14171-8 |
| Support Opportunities: | Scholarships in Brazil - Post-Doctoral |
| Start date: | February 01, 2023 |
| End date: | January 31, 2025 |
| Field of knowledge: | Health Sciences - Medicine - Pathological Anatomy and Clinical Pathology |
| Principal Investigator: | Claudia Kimie Suemoto |
| Grantee: | Alberto Fernando Oliveira Justo |
| Host Institution: | Faculdade de Medicina (FM). Universidade de São Paulo (USP). São Paulo , SP, Brazil |
Abstract Alzheimer's Disease (AD) is a progressive neurodegenerative disease, being the most frequent cause of dementia worldwide. Around 50 million people is estimated to have AD or other dementias and this number tends to double every 20 years. Although the etiology of the disease is partially explained by the deposition of aggregated forms of ²-amyloid proteins and neurofibrillary tangles in the brain, AD is a multifactorial disorder that involve genetic and environmental factors. In this context, the discovery of new pathways that are part of AD pathophysiology plays a vital role in discovering new treatments. Currently, there is growing interest in elucidating the role of the nitric oxide (NO) pathway in AD. Studies in animal models suggest that nitric oxide synthases (NOS) may be directly and indirectly involved in the AD pathophysiology. Neural, inducible and endothelial nitric oxide synthase (nNOS, iNOS, eNOS) may play an important role in the pathophysiology of AD through the promotion of oxidative stress in the brain. However, the expression of these enzymes in the human brain of individuals with AD has been underinvestigated. In this context, our objective is to characterize the expression of the nNOS, iNOS and eNOS enzymes and the protein nitrotyrosine (a metabolite of reactive species) in the hippocampus of individuals with AD through immunohistochemistry. To understand the relationship between NOS and oxidative stress and AD neuropathology, we will investigate the co-localization of NOS expression with nitrotyrosine, amyloid protein, and phosphorylated tau using immunofluorescence. Furthermore, to understand the regulation of antioxidant pathways, we will evaluate the expression of the enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) by RT-PCR. Finally, we will investigate the correlation between NOS levels and the clinical severity of AD. | |
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