The current models unravel the molecular mechanisms underlying the intricate pathophysiology of Alzheimer's disease using zebrafish.

Abstract

The foremost cause of dementia is Alzheimer's disease (AD). The vital pathological hallmarks of AD are amyloid beta (Aβ) peptide and hyperphosphorylated tau (p-tau) protein. The current animal models used in AD research do not precisely replicate disease pathophysiology, making it difficult for researchers to quickly and effectively gather data or screen potential therapy possibilities. Several transgenic animals are used as models for AD; however, they have cost and time concerns. Zebrafish (Danio rerio) has become a suitable model organism for high-throughput pharmacological screening of neuroactive substances and neurodegenerative research. The past few decades have seen a significant increase in research on AD. The fight against amyloidosis has, however, been unexpectedly unsuccessful. It may be due to a need for more relevant in vivo models for high throughput screening, which emphasizes the need to find other anti-AD models. Alternative animal models, including zebrafish, have developed into a potentially useful research tool that must be employed for AD research to be effective. Only a few comprehensive zebrafish models exhibiting AD-like pathogenesis have been reported in the literature, and this book chapter describes these models.