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Updated: Oct 27, 2025

Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke
Published on: March 22, 2016
Role of RhoA/ROCK signaling in Alzheimer's disease
RuoLan Cai1, YangYang Wang2, ZhenTing Huang2
1Zunyi Medical University, Zunyi, 563003, China; Department of Neurology, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, China; Chongqing Key Laboratory of Neurodegenerative Diseases, Chongqing, 400013, China; Department of Neurology, Chongqing General Hospital, University of Chinese Academy of Sciences, Chongqing, 400013, China.
Abstract:
Rho-associated coiled-coil kinase (ROCK), a serine/threonine kinase regulated by the small GTPase RhoA, is involved in regulating cell migration, proliferation, and survival. Numerous studies have shown that the RhoA/ROCK signaling pathway can promote Alzheimer's disease (AD) occurrence. ROCK activation increases β-secretase activity and promotes amyloid-beta (Aβ) production; moreover, Aβ further activates ROCK. This is suggestive of a possible positive feedback role for Aβ and ROCK. Moreover, ROCK activation promotes the formation of neurofibrillary tangles and abnormal synaptic contraction. Additionally, ROCK activation can promote the neuroinflammatory response by activating microglia and astrocytes to release inflammatory cytokines. Therefore, ROCK is a promising drug target in AD; further, there is a need to elucidate the specific mechanism of action.
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