Kefir como probiótico e fonte de metabólitos: um estudo em Drosophila melanogaster modelo da Doença de Alzheimer

• Ano de defesa: 2020
• Autor(a) principal: Batista, Leticia Leandro
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Uberlândia; Brasil; Programa de Pós-graduação em Genética e Bioquímica
• Palavras-chave em Português: Drosophila melanogaster; Doença de Alzheimer; Kefir; Probióticos; Disbiose; CNPQ::CIENCIAS BIOLOGICAS::GENETICA::GENETICA MOLECULAR E DE MICROORGANISMOS; CNPQ::CIENCIAS BIOLOGICAS::GENETICA; Alzheimer, Doença de; Metabólitos
• Link de acesso: https://repositorio.ufu.br/handle/123456789/30893; https://doi.org/10.14393/ufu.di.2020.770

Alzheimer’s Disease (AD) is the most common cause of dementia among elderly individuals worldwide, leading to a strong motor-cognitive decline and consequent emotional distress and codependence. It is traditionally characterized amyloidogenic pathway formation of senile plaques, and recent studies indicate that dysbiosis is also an important factor in AD’s pathology. To overcome dysbiosis, probiotics – as kefir – have shown to be a great therapeutic alternative for Alzheimer’s disease. In this present work, we explored kefir as a probiotic and a metabolite source as a modulator of microbiome and amyloidogenic pathway, using a Drosophila melanogaster model for AD (AD-like flies). Kefir microbiota composition was determined through 16S rRNA sequencing, and its metabolites were obtained through liquid-liquid partitioning with hexane, dichloromethane, ethyl acetate and n-butanol. After treatment, flies had its survival, climbing ability and eye morphology analyzed. Kefir treated flies improved both their climbing ability and survival rate, whereas flies treated with non-polar fractions improved the first and, the ones treated with polar fractions improved the second. In conclusion, we show that both kefir and its fractions may be promising therapeutic source against AD, through modulating amyloidogenic related pathways and gut dysbiosis.