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Investigation of the effects of cannabidiol (CBD) in an animal model of Alzheimer's Disease induced by streptozotocin

Grant number: 21/12409-7
Support type:Scholarships in Brazil - Master
Effective date (Start): March 01, 2022
Effective date (End): September 30, 2023
Field of knowledge:Biological Sciences - Pharmacology - Neuropsychopharmacology
Principal researcher:Alessandra Mussi Ribeiro
Grantee:Gabrielle Christine Pereira
Home Institution: Instituto de Saúde e Sociedade (ISS). Universidade Federal de São Paulo (UNIFESP). Campus Baixada Santista. Santos , SP, Brazil

Abstract

Alzheimer's Disease (AD) is a progressive neurodegenerative disorder and the most common cause of types of dementia in the elderly. Studies have pointed out as a possible mediator of neurodegeneration the early deficiency in brain glucose metabolism and insulin signaling pathway, consequently resulting in oxidative stress processes, increased production of A² peptide, Tau protein dysfunction, mitochondrial dysfunction, activation of molecules pro-inflammatory, activation of astrocytes and microglia, and cellular apoptosis. Currently, one of the main challenges is the development of drugs that prevent the progression and/or prevent the emergence of AD. In this context, bioactive compounds derived or isolated from plants may have antioxidant and anti-inflammatory activity and may have a neuroprotective effect in neurodegenerative diseases. The aim of this study is to investigate the potential neuroprotective effect of Cannabidiol Oil (CBD) in a pharmacological model of AD, induced by streptozotocin (STZ) in Wistar rats. For that, the animals will receive an injection of STZ (3 mg/kg, via i.c.v.) and will be treated with CBD (10 mg/kg, orally) for 14 days. Sucrose preference tests, open field, olfactory sensitivity, spontaneous alternation, and new object recognition tasks will be performed during the treatment. At the end of the treatment, the brains will be collected to perform immunohistochemistry for Ab and Tau and inflammatory cytokines (IL1b and IL-6) and dosages of oxidative stress parameters (lipid peroxidation and activity of the enzymes catalase, superoxide dismutase and glutathione peroxidase) in the brain areas of the olfactory bulb, hippocampus, and cerebral cortex. (AU)

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