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Related Experiment Video

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Age-dependent concomitant changes in synaptic dysfunction and GABAergic pathway in the APP/PS1 mouse model.

Tutu Oyelami1, An De Bondt2, Ilse Van den Wyngaert3

  • 1Department of Neuroscience, Janssen Research and Development, A Division of Janssen Pharmaceutica NV, Beerse, Belgium; Institute of Neuroscience, Université Catholique de Louvain, Louvain-La-Neuve, Belgium.

Acta Neurobiologiae Experimentalis
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Summary

Alzheimer's disease (AD) shows age-dependent synaptic dysfunction and altered GABAergic neurotransmission in aged APPPS1 mice. This imbalance in excitation and inhibition may explain AD symptoms like seizures and sleep disturbances.

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Area of Science:

  • Neuroscience
  • Pathology
  • Molecular Biology

Background:

  • Synaptic dysfunction is a hallmark of Alzheimer's disease (AD) pathology in animal models.
  • Increased neuronal excitability and seizures are observed in AD patients and models, seemingly contradicting reduced synaptic function.
  • This suggests a complex interplay between excitatory and inhibitory neuronal mechanisms in AD.

Purpose of the Study:

  • To investigate functional deficits in the inhibitory (GABAergic) system in AD.
  • To determine if GABAergic system deficits correlate with alterations in the glutamate excitatory pathway.
  • To explore the link between age-dependent synaptic dysfunction, excitation/inhibition imbalance, and AD progression.

Main Methods:

  • Utilized aged APPPS1 mouse models of Alzheimer's disease.
  • Assessed synaptic function and GABAergic neurotransmission.
  • Compared findings between younger and aged APPPS1 mouse cohorts.

Main Results:

  • Identified age-dependent changes in synaptic function in aged APPPS1 mice.
  • Observed alterations in GABAergic neurotransmission accompanying synaptic dysfunction.
  • Demonstrated an excitation/inhibition imbalance in aged AD models.

Conclusions:

  • Age-dependent alterations in the inhibitory/excitatory balance contribute to Alzheimer's disease progression.
  • Impaired GABAergic neurotransmission is a key factor in AD-related synaptic dysfunction.
  • This imbalance may underlie AD symptoms such as sleep disturbances and epileptic events.