4.6

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2.2

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  • ISSN 1674-8301
  • CN 32-1810/R
Wenting He, Xiuyu Shi, Zhifang Dong. The roles of RACK1 in the pathogenesis of Alzheimer's disease[J]. The Journal of Biomedical Research, 2024, 38(2): 137-148. DOI: 10.7555/JBR.37.20220259
Citation: Wenting He, Xiuyu Shi, Zhifang Dong. The roles of RACK1 in the pathogenesis of Alzheimer's disease[J]. The Journal of Biomedical Research, 2024, 38(2): 137-148. DOI: 10.7555/JBR.37.20220259

The roles of RACK1 in the pathogenesis of Alzheimer's disease

  • The receptor for activated C kinase 1 (RACK1) is a protein that plays a crucial role in various signaling pathways and is involved in the pathogenesis of Alzheimer's disease (AD), a prevalent neurodegenerative disease. RACK1 is highly expressed in neuronal cells of the central nervous system and regulates the pathogenesis of AD. Specifically, RACK1 is involved in regulation of the amyloid-β precursor protein processing through α- or β-secretase by binding to different protein kinase C isoforms. Additionally, RACK1 promotes synaptogenesis and synaptic plasticity by inhibiting N-methyl-D-aspartate receptors and activating gamma-aminobutyric acid A receptors, thereby preventing neuronal excitotoxicity. RACK1 also assembles inflammasomes that are involved in various neuroinflammatory pathways, such as nuclear factor-kappa B, tumor necrosis factor-alpha, and NOD-like receptor family pyrin domain-containing 3 pathways. The potential to design therapeutics that block amyloid-β accumulation and inflammation or precisely regulate synaptic plasticity represents an attractive therapeutic strategy, in which RACK1 is a potential target. In this review, we summarize the contribution of RACK1 to the pathogenesis of AD and its potential as a therapeutic target.
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