Maladi ya Alzheimer kele maladi mosi ya mpasi yina ke vandaka ti mutindu ya mbi ya kubumba baproteine, ke vandaka ti maladi ya kupola, mpi ke salaka nde baselile ya butomfu kusala ve mbote.
Bikalulu zole ya ntete ya maladi ya Alzheimer kele plaques ya beta-amyloïde (Aβ) mpi ba enchevêtrement neurofibrillaire (NFT) na butomfu.
Ba plaque ya beta-amyloïde ke basikaka ntangu ba enzymes ke zengaka bitini ya proteine yina ke salaka nde ba amyloïde kubasika (APP) sambu na kusala ba peptide ya Aβ.
Peptide yai ke vukanaka mpi ke salaka fibrille yina ke vandaka ve ti masa, yina ke vukanaka na nganda ya baselile ya butomfu, yo ke bebisaka mutindu baselile ke solulaka mpi ke fwaka baselile ya butomfu.
Bantu keyindulaka nde, kuvukana ya plaque ya Aβ kele mosi na kati ya mambu ya ntete yina kebasikaka na maladi ya Alzheimer, mpi yo lenda vanda mpi na kisina ya maladi ya butomfu.
Ba tangle ya neurofibrilles ke basikaka ntangu proteine tau ke kumaka ti fosforile mingi mpi ke salaka ba filamente ya mbi na kati ya baselile ya butomfu.
Ba-tube yai ya kele ti bima mingi ya ke sadisaka nitu na kusala kisalu na yo ke salaka nde ba-neurone kusala ve mbote.
Nsukansuka, ba neurone yina kebebaka kefwaka.
Maladi ya ntu ke vandaka mpi na bupusi na maladi ya Alzheimer.
Bima yina ke taninaka nitu ke salaka mambu ntangu plake ya Aβ mpi NFT ke vukana na kubasisaka ba cytokine yina ke salaka nde maladi kuyantika, yina lenda bebisa baselile ya butomfu.
Diaka, kele ti banzikisa ya ke monisa nde basusi ya ke salaka nde nitu kukuma ti bima mingi ya ke fwaka, kubeba ya mitochondrie, mpi kubeba ya glucose ke salaka nde maladi ya Alzheimer kukuma ngolo.
Mambu yai lenda sala nde baselile ya butomfu kusala ve mbote mpi kufwa, ebuna yo lenda kumisa maladi ngolo.
Na kutuba ya mbote, maladi ya Alzheimer kele mpasi mingi sambu na mambu mingi yina kepusaka bantu na kuvidisa mayele mpi na kuvila mambu yina bo vandaka kuyindula.
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Casadesus G, Moreira PI, Nunomura A, Siedlak SL, Bligh-Glover W, Balraj E, Petot G, Smith MA, Perry G: Indices of metabolic dysfunction and oxidative stress. Neurochem Res. , 32 (4-5): 717-22.
Candore G, Bulati M, Caruso C, Castiglia L, Colonna-Romano G, Di Bona D, Duro G, Lio D, Matranga D, Pellicanò M, Rizzo C, Scapagnini G, Vasto S: Inflammation, cytokines, immune response, apolipoprotein E, cholesterol, and oxidative stress in Alzheimer disease: therapeutic implications. Rejuvenation Res. , 13 (2-3): 301-13.
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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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