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Basic Science and Pathogenesis.

Alyson M Curry1, Katherine M Holleran1, Sara R Jones1

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Summary
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Alzheimer's disease (AD) mouse models show cognitive and social impairments linked to dopamine system dysfunction. Targeting dopamine pathways may help alleviate AD-related deficits.

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Area of Science:

  • Neuroscience
  • Neurodegenerative Diseases
  • Pharmacology

Background:

  • Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-β and tau pathologies.
  • Neuropsychiatric symptoms are early AD manifestations linked to disease progression.
  • Dopamine's role in AD pathophysiology is implicated but underexplored, particularly in disease progression.

Purpose of the Study:

  • Investigate the relationship between cognitive deficits and mesolimbic dopamine function in Tau P301S mice.
  • Examine dopamine system alterations in a mouse model of tauopathy.
  • Assess dopamine's role in Alzheimer's disease progression.

Main Methods:

  • Cognitive and behavioral assessments (novel object recognition, social interaction, sucrose preference) in Tau P301S mice at 3, 6, and 9 months.
  • Ex vivo fast-scan cyclic voltammetry in the nucleus accumbens core to evaluate mesolimbic dopamine function.
  • Comparison with APP/PS1 mice model.

Main Results:

  • Progressive cognitive and social impairments observed in Tau P301S mice starting at 3 months.
  • Reduced D2 receptor sensitivity correlated with cognitive deficits by 6 months.
  • Worsened impairments at 9 months with trending dopamine release/reuptake reductions and further D2 receptor sensitivity declines.
  • Similar deficits in behavior and dopamine function observed in APP/PS1 mice.

Conclusions:

  • Tau P301S mice exhibit progressive impairments correlating with mesolimbic dopamine dysfunction.
  • Dopamine dysregulation is relevant across multiple AD models (Tau P301S and APP/PS1).
  • Mesolimbic dopamine system dysfunction plays a role in AD; targeting dopamine pathways may offer therapeutic benefits.