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Título: Octovespin, a peptide bioinspired by wasp venom, prevents cognitive deficits induced by amyloid-β in Alzheimer’s disease mouse model
Autor(es): Camargo, Luana Cristina
Veras, Leticia Germina
Vaz, Gabriela
Souza, Adolfo Carlos Barros de
Mortari, Márcia Renata
E-mail do autor: mailto:mmortari@unb.br
Assunto: Alzheimer, Doença de
Peptídeos
Vespa - veneno
Data de publicação: 11-Mar-2022
Editora: Elsevier
Referência: CAMARGO, Luana Cristina et al. Octovespin, a peptide bioinspired by wasp venom, prevents cognitive deficits induced by amyloid-β in Alzheimer’s disease mouse model. Neuropeptides, v. 93, art. 102233, jun. 2022. DOI 10.1016/j.npep.2022.102233. Disponível em: https://www.sciencedirect.com/science/article/pii/S0143417922000087?via%3Dihub. Acesso em: 227 jul. 2022.
Abstract: Approximately 46.8 million people have been diagnosed worldwide with dementia, of which the most common type is Alzheimer’s disease (AD). Since the current AD treatment is incipient and limited, it is essential to develop new drugs to prevent AD. Considering that evolutionary pressure selected animal venom compounds that are very specific for a unique target, those can be a potential drug against AD. Octovespin was modified from occidentalin-1202, which is a peptide isolated from Polybia occidentalis wasp venom. In this context, this study evaluated the effect of treatment with octovespin against Amyloid-β (Aβ)-induced toxicity, which is postulated to be one of the main causes of AD, in both in vitro and in vivo tests. In vitro, octovespin was able to prevent Aβ aggregation in a ThT assay. In vivo, octovespin (0.15 nmol/animal) reverses memory impairment that is due to Aβ toxicity, in the Morris Water Maze and Novel Object Recognition Test. Our results suggested that octovespin is a potential drug for the treatment of AD, due to its ability to avoid Aβ aggregation in vitro and to prevent Aβ -induced memory deficit in mice.
DOI: https://doi.org/10.1016/j.npep.2022.102233
Versão da editora: https://www.sciencedirect.com/science/article/pii/S0143417922000087?via%3Dihub
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