Presentation Date: Feb 14, 2026
AGSA Abstract
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder linked to dementia. Clinical diagnosis of AD occurs in the mid to advanced disease stages when patients exhibit signs of memory loss or dementia. Likewise, in AD experimental models, animals are assessed in the mid to late stages when behavioral phenotypes are discernible. The goal of the current study was to detect medial prefrontal cortex (mPFC) encoding of temporal order recognition (TOR) tasks over a chronic duration before and after toxic or non-toxic amyloid beta (Aβ) lesioning (48 days). The current study deploys in vivo PFC recording in mice during TOR tasks to detect changes in putative PFC encoding of TOR tasks in naïve mice (baseline) and after toxic Aβ(25-35) or control Aβ(35-25) lesioning. TOR recognition index had a positive correlation with increasing firing rate (FR) of putative units during correct (old) object exploration intervals. Furthermore, the percentage distribution of putative units with increased FR during old object intervals was more than that of recent object intervals. Interestingly, in Aβ(25-35) ensembles, the positive correlation between TOR performance and pyramidal FR was lost. In addition, there was a reduction in the percentage of units with increased FR during old object exploration. The positive correlation between the FR and the recognition index was retained in control Aβ(35-25) ensembles. Taken together, our results showed that toxic Aβ lesioning affects TOR memory encoding by altering memory encoding patterns associated with object recognition and discrimination.
