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- W4200599648 abstract "Abstract The free fatty acid FFA3 receptor (FFA3R) belongs to the superfamily of G-protein-coupled receptors (GPCRs). In the intestine and adipose tissue, it is involved in the regulation of energy metabolism but its function in the brain is unknown. We aimed, first, to investigate the expression of the receptor in the hippocampus of Alzheimer disease (AD) patients at different stages of the disease and, second, to assess whether genetic inactivation of the Ffar3 gene could affect the phenotypic features of the APP swe mouse model. The expression of transcripts for FFA receptors in post mortem human hippocampal samples and in the hippocampus of wild-type and transgenic mice was analyzed by RT-qPCR. We generated a double transgenic mouse, FFA3R -/- /APP swe , to perform cognition studies and to assess, by immunoblotting, Aβ and tau pathologies and the differential expression of synaptic plasticity-related proteins.For the first time, the occurrence of the FFA3R in the human hippocampus and its overexpression, even in the first stages of AD, was demonstrated. Remarkably, FFA3R -/- /APP swe mice do not have the characteristic memory impairment of 12-month-old APP swe mice. Also, this newly generated transgenic line does not develop the most important Alzheimer’s disease (AD)-related features, such as amyloid beta (Aβ) brain accumulations and tau hyperphosphorylation. These findings are accompanied by increased levels of the insulin-degrading enzyme (IDE) and lower activity of the tau kinases GSK3β and Cdk5. We conclude that the brain FFA3R is involved in cognitive processes and its inactivation prevents AD-like cognitive decline and pathological hallmarks." @default.
- W4200599648 created "2021-12-31" @default.
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- W4200599648 date "2021-12-06" @default.
- W4200599648 modified "2023-09-28" @default.
- W4200599648 title "Genetic Inactivation of Free Fatty Acid Receptor 3 Impedes Behavioral Deficits and Pathological Hallmarks in the APP Swe Alzheimer’s Disease Mouse Model" @default.
- W4200599648 doi "https://doi.org/10.21203/rs.3.rs-1124827/v1" @default.
- W4200599648 hasPublicationYear "2021" @default.
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