Imikorere y'indwara ya Alzheimer (AD) ni inzira igoye irimo kwiyongera kwa poroteyine zidasanzwe, kubyimba no kwangirika kw'imyakura.
Ibimenyetso bibiri by'ingenzi bya AD ni ukuba mu bwonko harimo amyloid-beta (Aβ) plaques na neurofibrillary tangles (NFTs).
Amapaki ya beta-amyloid abaho iyo ibice bya poroteyine y'ibanze ya amyloid (APP) bigabanyijwemo na enzymes kugira ngo habeho peptides za Aβ.
Izi peptide zishyira hamwe zigakora uturemangingo tudashobora gushonga twirundanya hanze ya neurones, bibangamira itumanaho ry'ingirabuzimafatizo na neuronal bigatuma ipfa.
Kwiyongera kw'ibinure bya Aβ ni kimwe mu bintu bitangira kugaragara mu gihe umuntu arwaye indwara ya Alzheimer, kandi bivugwa ko bigira uruhare mu gutuma imyakura y'ubwonko igenda yangirika.
Imigaragarire ya Neurofibrillary ibaho iyo poroteyine ya tau ihindutse hyperphosphorylated maze ikora insinga zidasanzwe imbere mu mitsi.
Ibyo bintu by'uruvange bibangamira imikorere isanzwe ya mikoro, ari na yo ituma intangangabo itwara intungamubiri n'ibindi bintu.
Ibyo bintu by'uruvange amaherezo bituma utwo duce tw'ubwonko twicwa.
Kubabara bigira uruhare no mu mikorere y'indwara ya AD.
Sisitemu y'ubudahangarwa bw'umubiri yitabira kwiyongera kwa Aβ plaques na NFTs mu kurekura sitokine zitera kubyimba, bishobora kongera kwangirika kwa neurones.
Byongeye kandi, hari ibimenyetso byerekana ko umunaniro ukabije, imikorere mibi ya mitochondrial, no kwangirika kw'imisemburo ya glucose bigira uruhare mu ndwara ya Alzheimer.
Muri rusange, pathophysiology ya AD ni imikoranire igoye yibintu byinshi amaherezo biganisha ku igabanuka rigenda ritera imbere ryimikorere yimikorere no kwibagirwa biranga iyi ndwara.
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Proft J, Weiss N: Jekyll and Hide: The two faces of amyloid β. Commun Integr Biol. 2012, 5 (5): 405-7.
Whitehouse PJ, Hedreen JC, White CL, Price DL: Basal forebrain neurons in the dementia of Parkinson disease. Ann Neurol. 1983, 13 (3): 243-8.
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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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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