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Related Experiment Videos

APC/CCdh1-Rock2 pathway controls dendritic integrity and memory.

Verónica Bobo-Jiménez1,2, María Delgado-Esteban1,2, Julie Angibaud3

  • 1Institute of Biomedical Research of Salamanca, University Hospital of Salamanca, University of Salamanca, Consejo Superior de Investigaciones Científicas, 37007 Salamanca, Spain.

Proceedings of the National Academy of Sciences of the United States of America
|April 12, 2017
PubMed
Summary

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Deleting Cdh1 in neurons disrupts brain structure and function, leading to memory loss and neurodegeneration. Inhibiting Rho kinase 2 (Rock2) with fasudil reversed these effects, offering a potential Alzheimer's disease therapy.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • Neuronal morphology disruption is key in neurodegenerative diseases like Alzheimer's disease (AD).
  • The molecular drivers of these morphological changes remain largely unknown.
  • Cdh1 is a crucial cofactor for the anaphase-promoting complex/cyclosome (APC/C) ubiquitin ligase.

Purpose of the Study:

  • To investigate the role of Cdh1 in maintaining neuronal structure and function.
  • To identify molecular mechanisms linking Cdh1 to neurodegeneration.
  • To explore potential therapeutic strategies targeting Cdh1-regulated pathways.

Main Methods:

  • Postnatal deletion of Cdh1 in mouse neurons (Cdh1 conditional knockout, cKO).
  • Assessment of dendritic arborization, spine density, and synapse loss in the cortex and hippocampus.
Keywords:
APC/CCdh1Rockdendritememoryneurodegeneration

Related Experiment Videos

  • Measurement of Rho protein kinase 2 (Rock2) protein levels and activity.
  • Pharmacological inhibition of Rock activity using fasudil.

    • Main Results:

    • Cdh1 deletion in neurons disrupted dendrite arborization and caused spine/synapse loss.
    • Rock2, an APC/CCdh1 substrate, accumulated in Cdh1 cKO mice, correlating with AD pathology.
    • Fasudil treatment prevented dendritic disorganization, memory deficits, and neurodegeneration in Cdh1 cKO mice.

    Conclusions:

    • APC/CCdh1-mediated Rock2 degradation is essential for maintaining dendritic networks, memory, and neuronal survival.
    • Aberrant Rock2 accumulation contributes to neurodegeneration.
    • Pharmacological inhibition of Rock2 presents a promising therapeutic avenue for neurodegenerative disorders.