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Review
. 2022 Nov 24:9:101933.
doi: 10.1016/j.mex.2022.101933. eCollection 2022.

Experimentally induced animal models for cognitive dysfunction and Alzheimer's disease

Deepthi Rapaka  1 , Paul C Adiukwu  2 , Veera Raghavulu Bitra  2
Affiliations
Review

Experimentally induced animal models for cognitive dysfunction and Alzheimer's disease

Deepthi Rapaka et al. MethodsX. .

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterised pathologically by the presence of extracellular amyloid plaques and the intracellular neurofibrillary tangles, along with inflammation, and a compromised antioxidant system. Significant insights into the neurobiology to better understand the pathophysiology of AD and to evaluate the possibility of cutting-edge therapy strategies, can be obtained through the selection of a well-designed experimental animal model. From the transgenic to chemical/drug-induced models, none of them represents the complete picture of Alzheimer pathology and incidence of cognitive dysfunction. Researchers did not explain why one model was preferred over another, did not consider how the pathological phenomena were formed (spontaneously, experimentally, or by genetic manipulation), and did not address the traits of the species that affect the results. There is a lack of concordance between preclinical models and clinical trials that could be due to variety of reasons such as incomplete models, choice of animal species, lack of variability, and the validity of the models. To provide greater translation of preclinical AD studies to clinical trials proper designing of the model is essential. This review provides a brief recap ranging from animal doses to their induction mechanism and common limitations of the chemical-induced AD models. • Animal models may fail to replicate the exact pathology of the disease • Validity of the model is essential for proper translation of pathology from animal models to human disease • Appropriate induction doses need to be administered.

Keywords: Alzheimer's disease; Animal models; Induction dose; Validation.

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Conflict of interest statement

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Authors declare no conflict of interest.

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