Advances and Limitations of Rodent Models in Alzheimer’s Disease Pathogenesis and Therapeutics

Alzheimer’s disease (AD) is a neurodegenerative condition characterised by several markers and physiological manifestations. While Alzheimer’s disease affects millions of people throughout the world, the intricacy of the condition and the limits of experimental models have slowed the discovery of viable treatments. Rodent models helped researchers identify critical features of Alzheimer’s disease pathogenesis and test novel treatment strategies. This chapter gives a detailed summary of rodent models used in Alzheimer’s disease research, concentrating on the numerous types of transgenic, knock-in and knock-out models that replicate the genetic alterations linked with familial AD. We look into pharmacological and neurotoxin-induced models as well as infusion models, to imitate particular pathological characteristics of the disease. In these models, pathological assessments are essential for determining the development of amyloid plaque, hyperphosphorylation of tau and neuroinflammatory responses, immunohistochemistry, ELISA as well as synaptic marker investigations, all play significant contributions. Regardless of the benefits they provide, rodent models have substantial limitations in recreating the complete spectrum of human Alzheimer’s disease, notable the neurodegeneration and comorbidities present in sporadic AD. As a result, the research is shifting toward more advanced humanised models and gene-editing tools, such as CRISPR/Cas9, to eliminate the disparity between research on rodents and human therapeutic applications. This chapter finishes with a discussion of future AD research paths, highlighting the importance of improved models that combine environmental, genetic, and lifestyle components in order to better portray the complexity of AD. Rodent models are still in an angle to contribute significantly to our understanding of AD and the development of disease-transforming treatments by overcoming these constraints.