DOI: 10.38007/978-1-80053-529-9

Neurodegenerative diseases are a group of chronic neurological disorders characterized by progressive neuronal loss and synaptic dysfunction. These include Alzheimer's disease (AD), Parkinson's disease (PD), and Lewy body dementia. Their insidious onset, prolonged course, and extremely poor prognosis have made them a significant public health challenge in the context of a global aging population. With the continued increase in the proportion of the global elderly population, the incidence of neurodegenerative diseases is rising annually, causing severe cognitive impairment, motor dysfunction, and other physical and psychological suffering for patients, while also placing a heavy medical burden and care pressure on families and society. Currently, the pathogenesis of most neurodegenerative diseases is not fully understood, and effective early diagnostic methods and radical treatments are lacking. Therefore, in-depth research into the pathological characteristics and molecular mechanisms of these diseases, screening for specific biomarkers, and developing targeted therapeutic strategies have become research hotspots and urgent needs in the field of neuroscience. 

The pathological processes of neurodegenerative diseases are complex and diverse, involving abnormal changes at multiple molecular, cellular, and tissue levels. Among these, the pathological deposition of amyloid-β (Aβ) and tau protein are the most representative core pathological features, especially in Alzheimer's disease (AD). Aβ is a polypeptide fragment produced by the proteolytic hydrolysis of amyloid precursor protein. Under normal circumstances, it can be metabolized and cleared by the body. However, when metabolism is imbalanced, Aβ abnormally aggregates to form soluble oligomers and insoluble amyloid plaques. The latter, as one of the classic pathological markers of AD, is widely deposited in the cerebral cortex and hippocampus. The formation of amyloid plaques not only directly damages neurons and synaptic structures but also induces local inflammatory responses, disrupting nervous system homeostasis and further aggravating neuronal damage. Tau protein, closely related to Aβ pathology, is a microtubule-associated protein mainly distributed in neuronal axons. Under normal conditions, it maintains microtubule stability and participates in intracellular transport. However, under pathological conditions, tau protein undergoes hyperphosphorylation and abnormal aggregation, forming neurofibrillary tangles, leading to microtubule depolymerization, cytoskeleton destruction, and ultimately neuronal failure and death. Aβ pathology and tau protein pathology are not isolated phenomena; they interact and synergistically promote the progression of neurodegenerative diseases. The specific regulatory mechanisms involved remain a key area of current research.

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