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Mechanisms related to neurodegenerative diseases and the involvement of the cannabinoid system

Grant number: 14/06372-0
Support type:Regular Research Grants
Duration: August 01, 2014 - July 31, 2016
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Principal Investigator:Andréa da Silva Torrão
Grantee:Andréa da Silva Torrão
Home Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil


Neurodegenerative diseases are characterized by progressive loss of neurons in the central nervous system and, in general, have unknown etiology. Factors such as age, genetic and environmental, increased free radical formation, mitochondrial dysfunction, neuroinflammation, accumulation of neurotoxic factors, changes in the homeostasis of Ca2+ and in the energy metabolism may contribute to the development of the neurodegenerative process. In the last few years, several studies employing different experimental models of neurotoxicity and neuroinflammation have suggested neuroprotective properties of the cannabinoid system, with the participation of endo-and/or exocannabinoids and cannabinoid receptors CB1 and CB2 in these processes. However, the mechanisms underlying neuroprotection are unclear and the literature data are contradictory. The aim of this project is to evaluate the role of cannabinoid system in vivo and in vitro experimental models of neurodegeneration, investigating aspects related to oxidative stress, neuroinflammation, calcium and endoplasmic reticulum homeostasis, and the effects of treatment with cannabinoid compounds. We will use a model of neurodegeneration in vivo that reproduces some aspects of Alzheimer's disease in rats (intracerebroventricular injection of streptozotocin) and in vitro models in a neuronal cell line and primary cultures of neurons and glia. Parameters such as distribution of receptors, cell viability/proliferation, and production of reactive species will be evaluated, as well as approaches to elucidate possible mechanisms of action of cannabinoids, such as protein levels and gene expression. (AU)

Scientific publications (5)
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
CRUNFLI, FERNANDA; VRECHI, TALITA A.; COSTA, ANDRESSA P.; TORRAO, ANDREA S. Cannabinoid Receptor Type 1 Agonist ACEA Improves Cognitive Deficit on STZ-Induced Neurotoxicity Through Apoptosis Pathway and NO Modulation. NEUROTOXICITY RESEARCH, v. 35, n. 3, p. 516-529, APR 2019. Web of Science Citations: 2.
VRECHI, TALITA A.; CRUNFLI, FERNANDA; COSTA, ANDRESSA P.; TORRAO, ANDREA S. Cannabinoid Receptor Type 1 Agonist ACEA Protects Neurons from Death and Attenuates Endoplasmic Reticulum Stress-Related Apoptotic Pathway Signaling. NEUROTOXICITY RESEARCH, v. 33, n. 4, p. 846-855, MAY 2018. Web of Science Citations: 7.
PRIETO-ALMEIDA, FERNANDA; PANVELOSKI-COSTA, ANA CAROLINA; CRUNFLI, FERNANDA; TEIXEIRA, SILVANIA DA SILVA; NUNES, MARIA TEREZA; TORRAO, ANDREA DA SILVA. Thyroid hormone improves insulin signaling and reduces the activation of neurodegenerative pathway in the hippocampus of diabetic adult male rats. Life Sciences, v. 192, p. 253-258, JAN 1 2018. Web of Science Citations: 5.
CRUNFLI, FERNANDA; MAZUCANTI, CAIO HENRIQUE; MACEDO DE MORAES, RUAN CARLOS; COSTA, ANDRESSA PEREIRA; RODRIGUES, ALICE CRISTINA; SCAVONE, CRISTOFORO; TORRAO, ANDREA DA SILVA. NO-Dependent Akt Inactivation by S-Nitrosylation as a Possible Mechanism of STZ-Induced Neuronal Insulin Resistance. JOURNAL OF ALZHEIMER'S DISEASE, v. 65, n. 4, p. 1427-1443, 2018. Web of Science Citations: 2.
ZAMPIERI, THAIS TESSARI; OLIVEIRA DA SILVA, TIAGO EUGENIO; ROMEU, DEBORAH DE PAULA; TORRAO, ANDREA DA SILVA; DONATO, JR., JOSE. SOCS3 expression within leptin receptor-expressing cells regulates food intake and leptin sensitivity but does not affect weight gain in pregnant mice consuming a high-fat diet. Physiology & Behavior, v. 157, p. 109-115, APR 1 2016. Web of Science Citations: 3.

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