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Neuronal loss and brain atrophy in mice lacking cathepsins B and L

Ute Felbor1, Benedikt Kessler, Walther Mothes

  • 1Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA. felbor@biozentrum.uni-wuerzburg.de

Insights

Combined deficiency of cathepsins B and L in mice is lethal, causing severe brain atrophy and neurodegeneration. These cysteine proteases are crucial for maintaining central nervous system integrity.

Area of Science:

  • Biochemistry
  • Neuroscience
  • Molecular Biology

Background:

  • Cathepsins B and L are cysteine proteases involved in protein degradation and tissue remodeling.
  • Their specific in vivo functions, particularly in the central nervous system, require further elucidation.

Purpose of the Study:

  • To investigate the in vivo necessity of cathepsins B and L for mammalian survival and central nervous system maintenance.

Main Methods:

  • Generation of a double knockout mouse model lacking both cathepsin B and cathepsin L (Cathepsin B(-/-)/L(-/-)).
  • Phenotypic analysis of knockout mice, including survival rates, brain morphology, neuronal apoptosis, and cellular pathology.

Main Results:

  • Combined deficiency of cathepsins B and L resulted in early lethality (2-4 weeks of age).
  • Cathepsin B(-/-)/L(-/-) mice exhibited significant brain atrophy, characterized by massive neuronal apoptosis in the cerebral cortex and cerebellum.
  • Neurodegeneration was associated with reactive astrocytosis, axonal enlargements, and the accumulation of unique lysosomal bodies.

Conclusions:

  • Cathepsins B and L play a critical and indispensable role in the maintenance and survival of the central nervous system.
  • The study highlights a novel function of these proteases in preventing neurodegeneration.

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