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Alzheimer's disease (AD) is a common neurodegenerative disease characterized by neuritic plaques, neurofibrillary tangles, and neuroinflammation in the brain, accompanied by cognitive impairment and memory loss
Neuroinflammation regulation and β-amyloid (Aβ) production are key factors in the pathogenesis of Alzheimer's disease (AD)
Image credit: https://doi.
Recently, researchers from Beijing Institute of Technology published a paper entitled "Microglial cathepsin E plays a role in neuroinflammation and amyloid β production in Alzheimer's disease" in the journal Aging Cell.
In this study, we demonstrated that ablation of CatE significantly reduced Aβ accumulation, neuroinflammation, and cognitive impairment in human amyloid precursor protein knockout mice (appN LGF mice)
Furthermore, cannula-delivered CATE inhibitors improved memory function in AD mice and reduced Aβ accumulation and neuroinflammation
Elevated CATE levels in brain microglia of Alzheimer's disease patients
Image credit: https://doi.
Taken together, both lack of CATE and treatment with GV that inhibits CATE reduce neuroinflammation and Aβ accumulation in vivo
To date, little is known about the effects of CatE on AD pathology, and it was not until the discovery of GV that specific inhibitors of CatE were discovered
references
Zhen Xie et al.
