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P2‐162: EXERCISE‐LINKED FNDC5/IRISIN CORRECTS SYNAPTIC PLASTICITY AND MEMORY DEFECTS IN MOUSE MODELS OF ALZHEIMER'S DISEASE
Author(s) -
Lourenco Mychael V.,
Arancio Ottavio,
Ferreira Sergio Teixeira,
De Felice Fernanda Guarino
Publication year - 2019
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2019.06.2569
Subject(s) - fndc5 , neuroprotection , neuroscience , myokine , hippocampus , synaptic plasticity , medicine , endocrinology , long term potentiation , biology , receptor , skeletal muscle , microbiology and biotechnology , fibronectin , extracellular matrix
indicated by increased hippocampal reactive oxygen species (ROS) production (p<0.05; Figure 1) and brain malondialdehyde level. Microglial and astrocyte hyperactivation as indicated by morphological changes of these cells (p<0.05; Figure 1) was also found in ORX-rats treated with vehicle. In addition, ORX-rats treated with vehicle had hippocampal apoptosis and hippocampal dysplasticity with cognitive decline (p<0.05; Figure 1). Testosterone replacement, NAC, inulin, or a combined therapy equally ameliorated cognitive decline by improving gut dysbiosis, alleviating BBB dysfunction, decreasing hippocampal ROS and MDA level, decreasing hippocampal apoptosis, reducing microglia and astrocyte activity, leading to improve cognitive function. Conclusions: These findings suggested that testosterone deprivation caused cognitive decline. Testosterone replacement, NAC, inulin, and a combined therapy equally ameliorated the deleterious effects of testosterone deprivation in the brain.