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Related Experiment Videos

Cortical neuronal apoptosis in CADASIL.

Anand Viswanathan1, Francoise Gray, Marie-Germaine Bousser

  • 1Department of Neurology, Assistance Publique-Hôpitaux de Paris (AP-HP) Hôpital Lariboisière-Université Paris VII, Paris, France.

Stroke
|September 30, 2006
PubMed
Summary

Neuronal apoptosis, or programmed cell death, is implicated in cortical atrophy in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). This process correlates with lesion burden and brain volume reduction.

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Area of Science:

  • Neuroscience
  • Neuropathology
  • Genetics

Background:

  • Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a genetic disorder caused by NOTCH3 gene mutations.
  • CADASIL serves as a key model for studying pure vascular dementia.
  • Cortical atrophy is linked to cognitive decline in CADASIL, but its mechanism remains unclear.

Purpose of the Study:

  • To investigate the potential role of neuronal apoptosis in cortical atrophy within CADASIL.
  • To explore the relationship between apoptosis, subcortical ischemic lesions, and brain volume in CADASIL patients.

Main Methods:

  • Analysis of brain tissue from 4 deceased CADASIL patients (2 demented) and 3 non-CADASIL controls.
  • Immunohistochemistry using antibodies against activated caspase-3 to detect apoptosis.

Related Experiment Videos

  • In situ end labeling assays to identify DNA fragmentation.

    • Main Results:

    • Widespread neuronal apoptosis was observed in the cerebral cortex of all CADASIL patients, particularly in layers 3 and 5.
    • No significant apoptosis was detected in control subjects.
    • Apoptosis levels correlated positively with the extent of subcortical ischemic lesions and negatively with brain volume.

    Conclusions:

    • Neuronal apoptosis is likely involved in the cortical atrophy seen in CADASIL.
    • The extent of apoptosis appears related to the burden of subcortical ischemic lesions.
    • These findings suggest apoptosis as a potential therapeutic target for CADASIL and other small vessel diseases.