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Volume 5, Issue 4 (2025) – 5 articles
Cover Picture: Since the first report of Alzheimer’s disease (AD) in 1906, scientists have made remarkable progress in elucidating its molecular mechanisms, pathogenic processes, and core neuropathological features. However, effective therapeutic strategies for AD remain elusive, and the disease is still fundamentally incurable. The use of animal models constitutes a critical step in investigating pathological mechanisms and conducting preclinical experiments. With advances in transgenic technology, a variety of mouse models have been developed to replicate the pathological changes, as well as cognitive and motor impairments, observed in AD patients. These models have played a pivotal role in studying the pathogenesis of AD and screening potential therapeutic approaches. For example, the Tg2576 mouse model can simulate AD-related pathological alterations, including β-amyloid (Aβ) plaque deposition, neuroinflammation, and cognitive impairment. Nevertheless, mouse models have limitations in mimicking the complex pathology and clinical manifestations of human AD. In contrast, some medium- to large-sized animals in nature, such as canines and non-human primates (NHPs), can spontaneously develop AD-like pathological changes. For instance, NHPs exhibit high similarity to humans in terms of brain structure and function, and their spontaneous AD-like pathological changes provide a more human-relevant model for investigating AD pathogenesis and drug screening. This article elaborates on the pathological characteristics, clinical manifestations, advantages, and disadvantages of five distinct animal models (mouse, cat, dog, sheep and NHPs) in experimental research, thereby providing a reference for model selection in AD studies.
