Prominent tauopathy and intracellular β-amyloid accumulation triggered by genetic deletion of cathepsin D: implications for Alzheimer disease pathogenesis.

Also, confirming previous reports [ 17 ], CatD-KO mice exhibited highly significant elevations in a C-terminally truncated, caspase-cleaved form of tau strongly implicated in NFT formation in AD [ 45 ] (Fig. 3 D, E).

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