阿茲海默症嘅病理生理係複雜嘅過程 涉及異常蛋白質嘅累積,炎症,同埋神經元嘅功能失調.
阿茲海默症嘅兩個主要特徵係 腦部出現阿米洛伊德-β (Aβ) 斑塊同神經纖維
阿米洛伊德-β 斑塊係當阿米洛伊德前
呢啲
Aβ 斑塊嘅累積被認為係 AD 發展嘅最早嘅事件之一,而且被認為會促進神經退行過程.
當 tau 蛋白過度
呢啲
最終會導致受影響嘅神經細胞死亡
炎症喺AD病嘅病理生理學上亦有作用.
免疫系統對Aβ斑塊同NFT嘅累積作出反應,釋放前炎症性細胞因子,可以加劇神經細胞嘅損傷.
除此之外,有證據顯示氧化壓力,線粒體功能失調,同埋葡萄糖代謝受損 都會促成AD病理生理學.
呢啲因素可以導致神經元功能失調同埋死亡, 進一步加劇疾病過程.
总的来说,AD病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记忆力丧失,这是该疾病的特征.
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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