[HTML][HTML] Paroxetine ameliorates prodromal emotional dysfunction and late-onset memory deficit in Alzheimer's disease mice
PH Ai, S Chen, XD Liu, XN Zhu, YB Pan… - Translational …, 2020 - Springer
PH Ai, S Chen, XD Liu, XN Zhu, YB Pan, DF Feng, S Chen, NJ Xu, S Sun
Translational neurodegeneration, 2020•SpringerBackground Neuropsychiatric symptoms (NPS) such as depression, anxiety, apathy, and
irritability occur in prodromal phases of clinical Alzheimer's disease (AD), which might be an
increased risk for later developing AD. Here we treated young APP/PS1 AD model mice
prophylactically with serotonin-selective re-uptake inhibitor (SSRI) paroxetine and
investigated the protective role of anti-depressant agent in emotional abnormalities and
cognitive defects during disease progress. Methods To investigate the protective role of …
irritability occur in prodromal phases of clinical Alzheimer's disease (AD), which might be an
increased risk for later developing AD. Here we treated young APP/PS1 AD model mice
prophylactically with serotonin-selective re-uptake inhibitor (SSRI) paroxetine and
investigated the protective role of anti-depressant agent in emotional abnormalities and
cognitive defects during disease progress. Methods To investigate the protective role of …
Background
Neuropsychiatric symptoms (NPS) such as depression, anxiety, apathy, and irritability occur in prodromal phases of clinical Alzheimer’s disease (AD), which might be an increased risk for later developing AD. Here we treated young APP/PS1 AD model mice prophylactically with serotonin-selective re-uptake inhibitor (SSRI) paroxetine and investigated the protective role of anti-depressant agent in emotional abnormalities and cognitive defects during disease progress.
Methods
To investigate the protective role of paroxetine in emotional abnormalities and cognitive defects during disease progress, we performed emotional behaviors of 3 months old APP/PS1 mouse following oral administration of paroxetine prophylactically starting at 1 month of age. Next, we tested the cognitive, biochemical and pathological, effects of long term administration of paroxetine at 6 months old.
Results
Our results showed that AD mice displayed emotional dysfunction in the early stage. Prophylactic administration of paroxetine ameliorated the initial emotional abnormalities and preserved the eventual memory function in AD mice.
Conclusion
Our data indicate that prophylactic administration of paroxetine ameliorates the emotional dysfunction and memory deficit in AD mice. These neuroprotective effects are attributable to functional restoration of glutamate receptor (GluN2A) in AD mice.
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