病因可能是因為患者的腦部受損,
兩種主要的症狀是腦部存在β-粉狀蛋白 (Aβ) 斑塊和神經纖維結 (NFT).
粉狀蛋白-β斑塊是由酶分解成Aβ的過程中形成的.
化物會形成不溶性纖維, 在神經元外積聚,
據信是AD發病最早的事件之一, 也可能導致神經退行性.
形成神經纖維結的原因是當tau蛋白過度酸化,
微小管是運送神經元內營養和其他物質的重要管道.
造成這些神經元死亡.
炎症也會對阿茲海默症的病理生理起到一定的作用.
免疫系統對Aβ斑塊和NFT的累積會釋放促炎細胞因子,
還有其他證據顯示氧化壓力,線粒體功能障礙,
這些因素會導致神經元功能障礙及死亡,
病因與治療方式都不同, 病因與治療方式各異,
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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