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From stress to Alzheimer's: A circuit-based framework for prefrontal cognitive dysfunction.

Jee Hyun Yi1

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Stress and Alzheimer's disease (AD) impair cognitive functions by disrupting prefrontal cortex (PFC) circuits. Both conditions converge on shared molecular pathways, affecting specific neuron types and leading to cognitive deficits.

Keywords:
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Area of Science:

  • Neuroscience
  • Cognitive Science
  • Pathology

Background:

  • Working memory and cognitive flexibility deficits are early signs of Alzheimer's disease (AD) and stress.
  • Prefrontal cortex (PFC) circuits are crucial for these functions and are vulnerable to insults.
  • Both AD and stress impact specific molecular and cellular targets within neural populations.

Purpose of the Study:

  • To synthesize evidence on how stress and AD pathology converge on shared vulnerable pathways in the PFC.
  • To outline a framework for understanding cell-type-specific vulnerabilities.
  • To identify potential targets for enhancing cognitive resilience.

Main Methods:

  • Review of molecular, cellular, and circuit-level evidence.
  • Analysis of studies on chronic stress and AD models.
  • Examination of synaptic signaling pathways (NR2B-NMDA receptors, GSK-3β).

Main Results:

  • Stress and AD dysregulate NR2B-NMDA receptor signaling and GSK-3β activation.
  • These changes occur in a cell-type-specific manner, affecting pyramidal neurons and interneuron subtypes (SST+, PV+, VIP+).
  • Imbalance in neural excitation/inhibition disrupts PFC circuit integrity and impairs behavior.

Conclusions:

  • Stress and AD pathology converge on common molecular and cellular pathways within the PFC.
  • Understanding cell-type-specific vulnerabilities is key to developing targeted interventions.
  • This framework may inform strategies for enhancing cognitive resilience in neurodegenerative and stress-related disorders.