Pathophysiologie ya maladi ya Alzheimer (AD) ezali likambo moko ya mpasi oyo esangisi bokutani ya ba proteine ya mabe, inflammation, mpe dysfonctionnement ya neurones.
Bilembo mibale ya liboso ya maladi ya Alzheimer ezali plaque ya amyloïde-bêta (Aβ) mpe matonga ya ba neurones (NFT) na bɔɔngɔ.
Ba plaque ya beta-amyloïde ebotamaka ntango biteni ya proteine ya ebandeli ya amyloïde (APP) ekatanaka na ba enzymes mpo na kosala ba peptides ya Aβ.
Peptide oyo esanganaka mpe esalaka fibrille oyo ekoki kosila te oyo esanganaka na libanda ya neurone, mpe ebebisaka boyokani ya selile na selile mpe ememaka na liwa ya neurone.
Bato bakanisaka ete kobakisama ya baplakɛ ya Aβ ezali moko ya makambo ya liboso oyo ebandaka na maladi ya Alzheimer, mpe bakanisaka ete yango nde esalaka ete maladi yango ebebisa bɔɔngɔ.
Maboke ya neurofibrillary esalemaka ntango proteine tau ekomi hyperphosphorylée mpe ekomi ba filaments ya mabe na kati ya neurones.
Mwa biloko yango ebebisaka mosala ya malamu ya ba microtubules, oyo ezalaka na ntina mingi mpo na komema biloko oyo etongaka nzoto mpe biloko mosusu na kati ya neurone.
Nsukansuka, misisa yango oyo ekangamá ebomaka.
Kobima ya ba inflammation esalaka mpe mosala na pathophysiologie ya AD.
Systeme ya immunité eyanolaka na bokutani ya plaque ya Aβ mpe NFTs na kobimisama ya ba cytokines oyo epesaka maladi, oyo ekoki kobakisa mbeba na ba neurones.
Lisusu, ezali na bilembo oyo emonisi ete stress ya oxydation, dysfonctionnement ya mitochondria, mpe kobeba ya métabolisme ya glucose esalaka ete maladi ya Alzheimer ezala.
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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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