{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,7]],"date-time":"2026-11-07T23:02:28Z","timestamp":1794092548042,"version":"4.8.0"},"reference-count":151,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2025,3,20]],"date-time":"2025-03-20T00:00:00Z","timestamp":1742428800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000049","name":"National Institute on Aging","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Aging"],"abstract":"<jats:p>Alzheimer\u2019s disease (AD) is the most common age-related neurodegenerative disease and cause of dementia. AD pathology primarily involves the formation of amyloid \u03b2 (A\u03b2) plaques and neurofibrillary tangles containing hyperphosphorylated tau (p-tau). While A\u03b2 targeted treatments have shown clinical promise, other aspects of AD pathology such as microgliosis, astrocytosis, synaptic loss, and hypometabolism may be viable targets for treatment. Among notable novel therapeutic approaches, the Ras homolog (Rho)-associated kinases (ROCKs) are being investigated as targets for AD treatment, based on the observations that ROCK1\/2 levels are elevated in AD, and activation or inhibition of ROCKs changes dendritic\/synaptic structures, protein aggregate accumulation, inflammation, and gliosis. This review will highlight key findings on the effects of ROCK inhibition in A\u03b2 and ptau pathologies, as well as its effects on neuroinflammation, synaptic density, and potentially metabolism and bioenergetics.<\/jats:p>","DOI":"10.3389\/fragi.2025.1547883","type":"journal-article","created":{"date-parts":[[2025,3,20]],"date-time":"2025-03-20T09:19:00Z","timestamp":1742462340000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":12,"title":["Rock inhibitors in Alzheimer\u2019s disease"],"prefix":"10.3389","volume":"6","author":[{"given":"Chao","family":"Zheng","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Weiming","family":"Xia","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jianhua","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2025,3,20]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"97","DOI":"10.1186\/s13195-017-0320-4","article-title":"Rho GTPases as therapeutic targets in Alzheimer\u2019s disease","volume":"9","author":"Aguilar","year":"2017","journal-title":"Alzheimers Res. 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