Amyloid-β alters medial prefrontal cortex encoding of temporal order task.

Area of Science:

• Neuroscience
• Cognitive Science

Background:

• Alzheimer's disease (AD) is a progressive neurodegenerative disorder causing dementia.
• Clinical and experimental diagnoses of AD occur late, when symptoms are evident.

Purpose of the Study:

• Investigate temporal order recognition (TOR) encoding in the medial prefrontal cortex.
• Examine changes during chronic toxic or non-toxic amyloid-beta (Aβ) lesioning over 48 days.

Main Methods:

• Utilized *in vivo* electrophysiological recordings in the medial prefrontal cortex.
• Monitored putative pyramidal cell firing rates during TOR tasks.
• Administered toxic Aβ25-35 or control Aβ35-25 lesions.

Main Results:

• TOR performance correlated positively with unit firing rate changes during old object exploration.
• Increased firing rates were more prevalent during old vs. recent object intervals.
• Toxic Aβ25-35 lesions abolished the TOR performance-firing rate correlation and reduced unit activity during old object exploration.

Conclusions:

• Toxic Aβ lesioning disrupts TOR memory encoding by altering medial prefrontal cortex ensemble activity.
• Impaired object recognition and discrimination patterns were observed following toxic Aβ exposure.
• Control Aβ lesions maintained a positive correlation between unit firing rate and recognition memory.