Alzheimer’s disease (AD) is the leading neurodegenerative disorder affecting the world’s
elderly population. Most experimental models of AD are transgenic or pharmacological in nature, and
do not simulate the entire pathophysiology. In the present study, we developed a pharmacologically
induced AD using the zebrafish, a species that can recapitulate most of the phenotypes of the disease.
The pharmacological agent being used, okadaic acid (OKA) has also been utilized to study AD in
other species. In this model, the immunohistochemistry of phosphorylated glycogen synthase-3α/β,
Aβ, p-tau, tau protein, and senile plaque formation in zebrafish brain were all significantly increased with increasing
exposure to OKA. These represent the majority of the histological hallmarks of AD pathophysiology. The observed
changes were also accompanied by learning and memory deficits which are also important components in AD
pathophysiology. Zebrafish disease models are gaining popularity mostly due to their economic cost and relevance to
human disease pathophysiology. Current pharmacological methods of inducing AD in zebrafish are not adequately
developed and do not represent all the features of the disease. OKA-induced AD in zebrafish can become a cost efficient
model to study drug discovery for AD. It may also be used to unravel the molecular mechanisms underlying the complex
pathophysiology that leads to AD using relatively economical species.
Keywords: Okadaic acid, Alzheimer’s Disease, Zebrafish, Tau & phospho-Tau protein, Amyloid β, glycogen synthase-3α/β &,
phospho-GSK-3α/β, senile plaque.
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