Abstract
Rodent models have been extensively used to investigate the cause and mechanisms behind Alzheimer’s disease. Despite many years of intensive research using these models we still lack a detailed understanding of the molecular events that lead to neurodegeneration. Although zebrafish lack the complexity of advanced cognitive behaviors evident in rodent models they have proven to be a very informative model for the study of human diseases. In this review we give an overview of how the zebrafish has been used to study Alzheimer’s disease. Zebrafish possess genes orthologous to those mutated in familial Alzheimer’s disease and research using zebrafish has revealed unique characteristics of these genes that have been difficult to observe in rodent models. The zebrafish is becoming an increasingly popular model for the investigation of Alzheimer’s disease and will complement studies using other models to help complete our understanding of this disease.
Highlights
Rodent models have been extensively used to investigate the cause and mechanisms behind Alzheimer’s disease
There is significant neuronal loss in several brain regions in Alzheimer’s disease (AD) patients (Regeur et al, 1994; West et al, 1994). This is usually accompanied by extracellular aggregates of the amyloid-beta peptide and intracellular aggregates of the tau protein called neurofibrillary tangles (NFTs)
FAD is attributed to mutations in three genes, PRESENILIN 1 (PSEN1), PRESENILIN 2 (PSEN2), and the AMYLOID BETA A4 PRECURSOR PROTEIN (APP)
Summary
Rodent models have been extensively used to investigate the cause and mechanisms behind Alzheimer’s disease. Zebrafish embryos injected with a psen1 translation-blocking morpholino are viable and have similar phenotypes (Nornes et al, 2003; Campbell et al, 2006; Nornes et al, 2008) to Psen1−/− mice such as aberrant somite formation and Notch signaling defects (Shen et al, 1997; Wong et al, 1997) Interestingly, a zebrafish mutant (discovered in a TILLING screen) lacking Psen1 activity is viable (Sundvik et al, 2013).
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