A study investigating the role of cathepsin D (CTSD) in neuroprotection has provided compelling evidence of its critical importance in preventing neurodegenerative processes.

The central idea of the work is that overexpression of CTSD can compensate for the deficiency of this enzyme caused by genetic knockout, thereby preventing the development of lethal consequences and the accumulation of amyloid plaques characteristic of neurodegenerative diseases such as Alzheimer's disease.

Lysosomes, intracellular organelles, play a key role in the degradation of proteins and other cellular components, thereby ensuring cellular homeostasis. Cathepsins, including CTSD, are the most important lysosomal proteases responsible for the breakdown of various substrates, including toxic protein aggregates. CTSD deficiency in humans leads to the development of neurolipofuscinosis (NCL), a group of severe inherited neurodegenerative diseases characterized by the accumulation of lipofuscin in nerve cells and progressive neuronal damage. This disease demonstrates a direct link between lysosomal protease deficiency and the development of neurodegeneration.

Transgenic mouse, Cathepsin D, Mitochondrial bioenergetics

Z. Gan-Or, PA Dion, GA Rouleau

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