Arrestins are multifunctional proteins that regulate G-protein-coupled receptor (GPCR) signaling, desensitization, and internalization. The arrestin family includes four subtypes: visual arrestin1, β-arrestin1, β-arrestin2, and visual arrestin-4. Recent studies have revealed that β-arrestins have additional roles beyond GPCR signaling, including scaffolding and adapter functions, and interactions with non-GPCR receptors. β-arrestins are involved in the pathogenesis of various neurodegenerative diseases, such as Alzheimer's disease (AD), frontotemporal dementia (FTD), and Parkinson's disease (PD). In AD, β-arrestins physically interact with γ-secretase, leading to increased amyloid-beta production and accumulation. In FTD, β-arrestin oligomers inhibit the autophagy cargo receptor p62/SQSTM1, causing tau accumulation and aggregation. In PD, β-arrestins are upregulated in postmortem brain tissue and an MPTP model, and the β2AR regulates SNCA gene expression. This review provides an overview of β-arrestin1 and β-arrestin2, their physiological functions, and their roles in neurodegenerative diseases. The multifaceted roles of β-arrestins suggest that they may serve as promising therapeutic targets.Arrestins are multifunctional proteins that regulate G-protein-coupled receptor (GPCR) signaling, desensitization, and internalization. The arrestin family includes four subtypes: visual arrestin1, β-arrestin1, β-arrestin2, and visual arrestin-4. Recent studies have revealed that β-arrestins have additional roles beyond GPCR signaling, including scaffolding and adapter functions, and interactions with non-GPCR receptors. β-arrestins are involved in the pathogenesis of various neurodegenerative diseases, such as Alzheimer's disease (AD), frontotemporal dementia (FTD), and Parkinson's disease (PD). In AD, β-arrestins physically interact with γ-secretase, leading to increased amyloid-beta production and accumulation. In FTD, β-arrestin oligomers inhibit the autophagy cargo receptor p62/SQSTM1, causing tau accumulation and aggregation. In PD, β-arrestins are upregulated in postmortem brain tissue and an MPTP model, and the β2AR regulates SNCA gene expression. This review provides an overview of β-arrestin1 and β-arrestin2, their physiological functions, and their roles in neurodegenerative diseases. The multifaceted roles of β-arrestins suggest that they may serve as promising therapeutic targets.