Abstract
Neurodegenerative disease (NDD), including Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis, are characterized by the progressive loss of neurons which leads to the decline of motor and/or cognitive function. Currently, the prevalence of NDD is rapidly increasing in the aging population. However, valid drugs or treatment for NDD are still lacking. The clinical heterogeneity and complex pathogenesis of NDD pose a great challenge for the development of disease-modifying therapies. Numerous animal models have been generated to mimic the pathological conditions of these diseases for drug discovery. Among them, zebrafish (Danio rerio) models are progressively emerging and becoming a powerful tool for in vivo study of NDD. Extensive use of zebrafish in pharmacology research or drug screening is due to the high conserved evolution and 87% homology to humans. In this review, we summarize the zebrafish models used in NDD studies, and highlight the recent findings on pharmacological targets for NDD treatment. As high-throughput platforms in zebrafish research have rapidly developed in recent years, we also discuss the application prospects of these new technologies in future NDD research.
Highlights
Neurodegenerative disease (NDD), including Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS), are progressive disorders with abnormal protein deposition and selective neuronal loss, leading to motor, and/or cognitive impairments and inevitable death (Vaquer-Alicea and Diamond, 2019)
A number of pharmacological drugs designed for NDD treatment have failed in clinical trials over the past several decades due to the clinical heterogeneity of the disease
Diseasemodifying treatments can only be effective in the early stage of the disease because most NDD pathologies are irreversible
Summary
Neurodegenerative disease (NDD), including Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS), are progressive disorders with abnormal protein deposition and selective neuronal loss, leading to motor, and/or cognitive impairments and inevitable death (Vaquer-Alicea and Diamond, 2019). Studies have been conducted to develop nanomedicine against AD or human amyloid diseases and the zebrafish model has been used for economic and high-throughput drug screening. A recent study found that insufficient expression of human α-syn can amplify cytoplasmic peroxide flux and oxidative stress, causing motor abnormalities prior to neuronal loss (Kang et al, 2018; Van Laar et al, 2020).
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