Amyloid-β and Neurodegeneration: Pathological Mechanisms and Therapeutic Challenges in Alzheimer’s Disease

Alzheimer's Disease (AD) is a common neurodegenerative disease and one of the leading causes of dementia. The prevalence of AD continues to rise globally, with the number of sufferers expected to exceed 139 million by 2050. The core pathological features of AD include beta-amyloid (Aβ) deposition, abnormal phosphorylation of Tau protein, synaptic dysfunction, and neuroinflammation. Among them, the abnormal metabolism of Aβ is considered to be the key pathogenic factor of AD, and the amyloid plaques formed by its accumulation can disrupt neuronal signaling, induce neuroinflammation, and accelerate neurodegeneration. In addition, the interaction of Aβ with Tau protein intensifies the formation of neurofibrillary tangles (NFTs), further impairs nerve function. In terms of early diagnosis, advances have been made in the study of Aβ-related biomarkers, including positron emission tomography (PET) imaging, cerebrospinal fluid and blood testing, and multi-omics analysis techniques, which provide new tools for early detection and accurate diagnosis of AD. At the same time, there is growing interest in strategies to prevent AD, such as a healthy diet, regular exercise, cognitive training, and chronic disease management, which may help reduce the risk of developing the disease. This article reviews the mechanism of Aβ in AD, and discusses the treatment and prevention strategies based on Aβ, in order to provide new ideas for the early diagnosis, precise treatment and multi-target intervention of AD.