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Reduced Prefrontal-Thalamic Theta Flow During Working Memory Retrieval in APP/PS1 Mice.

Shengnan Zhang1, Hongrui Ai1, Jia Wang1

  • 1School of Biomedical Engineering and Technology, Tianjin Medical University, Tianjin, China.

Journal of Alzheimer'S Disease : JAD
|February 2, 2024
PubMed
Summary
This summary is machine-generated.

Working memory retrieval is impaired in Alzheimer's disease (AD). In AD model mice, information flow from the medial prefrontal cortex to the mediodorsal thalamus significantly decreased during memory retrieval.

Keywords:
Alzheimer’s diseaseinformation flowlocal field potentialsmedial prefrontal cortexmediodorsal thalamusspatial working memory

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Area of Science:

  • Neuroscience
  • Cognitive Science
  • Biomedical Research

Background:

  • Working memory deficits are a hallmark of Alzheimer's disease (AD), impacting memory retrieval.
  • The precise mechanisms underlying impaired working memory retrieval in AD remain under-investigated.

Purpose of the Study:

  • To investigate functional interactions and information transmission between the medial prefrontal cortex (mPFC) and mediodorsal thalamus (MD) in a mouse model of AD.
  • To elucidate the role of mPFC-MD communication in memory retrieval processes affected by AD.

Main Methods:

  • Utilized a T-maze spatial working memory task in APP/PS1 transgenic mice and wild-type controls.
  • Recorded local field potentials (LFPs) from the mPFC and MD to analyze oscillatory activity and information flow.
  • Assessed temporal dynamics of neural activity and bidirectional information transfer during different task phases.

Main Results:

  • A significant reduction in theta-band information flow from the mPFC to the MD was observed in APP/PS1 mice compared to controls during memory retrieval.
  • Alterations in oscillatory activity and functional connectivity were identified between the mPFC and MD in the AD model.

Conclusions:

  • The mPFC-MD pathway plays a critical role in memory retrieval.
  • Disrupted information transfer from the mPFC to the MD is a potential underlying mechanism for working memory deficits observed in Alzheimer's disease models.