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Cathepsin B (CTSB) is involved in key pathological processes of AD, but the underlying mechanisms and its relevance to AD diagnosis and treatment remain unclear. In the present study, we found that CTSB expression was abnormally elevated in the hippocampus of 3\u00d7Tg mice and was regulated by miR\u201096\u20105p. Abnormalities in the miR\u201096\u20105p\/CTSB signaling pathway were detected in the serum of both mild cognitive impairment and AD patients, and the combination of serum miR\u201096\u20105p and CTSB demonstrated strong diagnostic efficacy for cognitive impairment (AUC = 0.7536). Abnormalities in the miR\u201096\u20105p\/CTSB signaling pathway in AD may be associated with A\u03b2 pathology, and neuronal CTSB can be released extracellularly to reactivate adjacent astrocytes. Ultimately, the reconstitution of the miR\u201096\u20105p\/CTSB signaling pathway effectively rescued astrocyte reactivity and memory impairment in AD. Our findings suggest that the neuron\u2010derived inflammatory mediator CTSB reactivates adjacent astrocytes and mediates memory impairment in early AD. The combination of serum miR\u201096\u20105p and CTSB represents potential serum biomarkers for cognitive impairment, and targeting the neuronal miR\u201096\u20105p\/CTSB pathway may serve as a promising therapeutic strategy for AD.<\/jats:p>","DOI":"10.1002\/mco2.70368","type":"journal-article","created":{"date-parts":[[2025,9,6]],"date-time":"2025-09-06T07:46:59Z","timestamp":1757144819000},"source":"Crossref","is-referenced-by-count":3,"title":["Targeting the miR\u201096\u20105p\/Cathepsin B Pathway to Alleviate Neuron\u2010Derived Neuroinflammation in Alzheimer's Disease"],"prefix":"10.1002","volume":"6","author":[{"given":"Kai","family":"Zheng","sequence":"first","affiliation":[{"name":"Department of Geriatrics Tongji Hospital Tongji Medical College Huazhong University of Science and Technology  Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"He\u2010Zhou","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Pathophysiology 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