Alzheimer's disease is defined by abnormal Aβ peptide and tau accumulation, with familial cases linked to mutations in APP, PSEN1, and PSEN2 genes. Immunotherapy targeting Aβ shows promise in delaying AD progression.
Aβ and tau form oligomers and protofibrils before accumulating into plaques and tangles in AD brains. Aβ plaques vary in morphology, while different types of tau filaments deposit within neurons in AD.
In AD, tau pathology correlates with neuronal loss and cognitive decline progression. Aβ 1-42 is a major constituent of AD β-amyloid, and mutations in tau-associated genes lead to other neurodegenerative diseases.
While Aβ deposits in amyloid plaques, tau filaments form tangles and threads within neurons in AD brains, showcasing different patterns of aggregation and deposition in the disease progression.
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