阿尔茨海默病的病理生理学是一个复杂的过程,涉及异常蛋白质的积累,炎症和神经元功能障碍.
艾滋病的两个主要特征是大脑中存在
当Amyloid前体蛋白 (APP) 的碎片被酶分裂形成Aβ
这些
据认为Aβ斑块的积累是AD发育的最早事件之一,并被认为有助于神经退行过程.
当蛋白质tau过度磷酸化并形成神经元内部的异常纤维时,神经纤维纠结会形成.
这些纠结破坏了微管的正常功能, 这些微管对于神经元内的营养物质和其他物质的运输至关重要.
这些纠结最终导致受影响的神经元死亡.
炎症在AD的病理生理学中也起着作用.
免疫系统通过释放促炎性细胞因子来应对Aβ斑块和NFT的积累,这可以加剧神经元的损伤.
此外,有证据表明氧化应激,线粒体功能障碍和葡萄糖代谢障碍有助于AD的病理生理学.
这些因素可能会导致神经元功能障碍和死亡,进一步加剧疾病过程.
总的来说,AD的病理生理学是多个因素的复杂相互作用,最终导致认知功能的逐渐下降和疾病的特征的记忆力损失.
PubMed/Medline https://www.nlm.nih.gov/databases/download/pubmed_medline.html
RefinedWeb https://arxiv.org/abs/2306.01116
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The pathophysiology of Alzheimer's disease (AD) is a complex process that involves the accumulation of abnormal proteins, inflammation, and neuronal dysfunction.
The two main hallmarks of AD are the presence of amyloid-beta (Aβ) plaques and neurofibrillary tangles (NFTs) in the brain.
Amyloid-beta plaques are formed when fragments of the amyloid precursor protein (APP) are cleaved by enzymes to form Aβ peptides.
These peptides aggregate and form insoluble fibrils that accumulate outside neurons, disrupting cell-to-cell communication and leading to neuronal death.
The accumulation of Aβ plaques is thought to be one of the earliest events in the development of AD, and it is believed to contribute to the neurodegenerative process.
Neurofibrillary tangles are formed when the protein tau becomes hyperphosphorylated and forms abnormal filaments inside neurons.
These tangles disrupt the normal functioning of the microtubules, which are essential for the transport of nutrients and other materials within the neuron.
The tangles eventually lead to the death of the affected neurons.
Inflammation also plays a role in the pathophysiology of AD.
The immune system responds to the accumulation of Aβ plaques and NFTs by releasing pro-inflammatory cytokines, which can exacerbate the damage to neurons.
Additionally, there is evidence that oxidative stress, mitochondrial dysfunction, and impaired glucose metabolism contribute to the pathophysiology of AD.
These factors can lead to neuronal dysfunction and death, further exacerbating the disease process.
Overall, the pathophysiology of AD is a complex interplay of multiple factors that ultimately lead to the progressive decline in cognitive function and memory loss that characterizes the disease.
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