Rodent Models for Alzheimer Disease: Experimental Induction, Pathophysiological Mechanisms, and Biomarker Profiling

Background Alzheimer’s disease (AD), the most common neurodegenerative disorder, is driven by amyloid-beta (Aβ) plaques, neurofibrillary tangles (NFTs), neuroinflammation, and oxidative stress. Rodent models are critical for studying its multifactorial etiology, combining genetic, environmental, and epigenetic factors. This review evaluates rodent AD models, including chemical induction (e.g., aluminum, scopolamine) and transgenic systems (e.g., 5xFAD, APP/PS1). Chemical models mimic sporadic AD triggers, while transgenics replicate genetic mutations. Combinatorial approaches (e.g., toxin- exposed transgenics) address limitations. Biomarkers such as Aβ/tau ratios, neuroinflammatory cytokines (TNF-α, IL-1β), and oxidative stress markers (MDA, SOD) validate pathology, measured via ELISA, PET imaging, and omics technologies.