Pathophysiology de maladi alzayme a (AD) se yon pwosesis konplèks ki enplike akimilasyon pwoteyin nòmal, enflamasyon, ak dysfonctionnement neuronal.
De mak prensipal yo nan AD se prezans nan plak amyloid-beta (Aβ) ak anmele neurofibrillary (NFTs) nan sèvo a.
Amyloid-beta plak yo fòme lè fragman pwoteyin amyloid précurseur (APP) yo fann pa anzim pou fòme Aβ peptides.
Peptides sa yo agrégées ak fòm fibril insoluble ki accumulent deyò neurones, interrompre sèlil-a-selil kominikasyon ak mennen a neuronal lanmò.
Akimilasyon plak Aβ yo panse se youn nan premye evènman nan devlopman AD, e yo kwè ke li kontribye nan pwosesis nerodegeneratif la.
Neurofibrillary tangles yo te fòme lè tau pwoteyin vin hyperphosphorylated ak fòm nòmal filaments anndan neurones.
Sa yo anmele deranje nòmal fonksyònman microtubules, ki esansyèl pou transpò eleman nitritif ak lòt materyèl nan a newòn.
Anfen, anmele yo lakòz newòn ki afekte yo mouri.
Enflamasyon jwe yon wòl tou nan patofizyoloji AD.
Sistèm iminitè a reponn ak akimilasyon plak Aβ ak NFTs pa divilge sitokin pro-enflamatwa, ki ka agrave domaj nan newòn yo.
Anplis de sa, gen prèv ke estrès oksidatif, mitokondriyo malfonksyònman, ak metabolis glikoz ki gen pwoblèm kontribye nan patofizyoloji AD.
Faktè sa yo ka mennen a dysfonctionnement neuronal ak lanmò, pli lwen aggraver pwosesis maladi a.
An jeneral, patofizyoloji de AD se yon entèaksyon konplèks de faktè miltip ki finalman mennen a progressive bès nan fonksyon kognitif ak memwa pèdi ki caractérise maladi a.
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What is pathophysiology of alzheimer?
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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