Alzheimer ƒe dɔlélea nye dɔ sesẽ aɖe si me lãmetsi siwo gblẽa nu le ame ƒe lãmenusese ŋu, kple lãmenugbagbevi siwo wɔa dɔ nyuie ƒe dɔwɔwɔ gblẽna le.
Nusiwo koŋ dea dzesi Alzheimer dɔléleae nye amyloid-beta (Aβ) ƒe kpeƒewo kple lãmeka siwo wɔa dɔ le ahɔhɔ̃a me ƒe ƒuƒoƒo (NFTs) si nɔa ahɔhɔ̃a me.
Amyloid-beta plaques dona ne lãmetsiwo gbã protein si nye amyloid ƒe gɔmedzeɖenua (APP) be wòazu Aβ peptides.
Peptide siawo ƒoa ƒu va zua lãmeka siwo meɖea ta o siwo va nɔa lãmenugbagbeviwo ŋu le gota, eye esia gblẽa nu le lãmenugbagbeviwo dome kadodo ŋu eye wònana lãmenugbagbeviawo kuna.
Wobui be Aβ-plaquewo ƒe ƒuƒoƒo nye nu gbãtɔ siwo naa Alzheimer-dɔlélea dzea egɔme la dometɔ ɖeka, eye wosusui be enana lãmekawo gblẽna.
Neurofibrillary tangles nyea protein si woyɔna be tau ƒe akpa aɖe si me nu siwo nana ame ƒe ahɔhɔ̃ wɔa dɔ nyuie la sɔa gbɔ ɖo fũu akpa eye wòzua lãmeka siwo me nu gblẽna le le ahɔhɔ̃a me.
Nu siawo gblẽa nu le lãmenugbagbevi sue siwo wɔa dɔ nyuie le lãmenugbagbevia me, siwo hiã vevie na nunyiamewo kple nu bubuwo tsɔtsɔ yi lãmenugbagbevia me la ŋu.
Mlɔeba la, lãmenugbagbevi siwo ŋu wògblẽ nu le la kuna.
Dɔléle sia ƒe dɔléle hã nye dɔ si nana ame léa dɔ.
Dɔlélenutsiŋutete wɔa nu ɖe Aβ kple NFT ƒe ƒuƒoƒo ŋu to lãmetsi siwo nana dɔléle nu sẽna la ɖeɖeɖa me, si ate ŋu ana lãmenugbagbeviwo nagblẽ ɖe edzi.
Gakpe ɖe eŋu la, kpeɖodziwo li be nu siwo hea dɔléle vɛ dometɔ aɖewoe nye nu siwo nana lãmetsiwo wɔa dɔ ɖe ame dzi, lãmenugbagbevi siwo nana lãmetsiwo wɔa dɔ nyuie o, kple sukli ƒe dɔwɔwɔ si megadzena nyuie o.
Nu siawo ate ŋu ana lãmekawo nagbe dɔwɔwɔ eye woaku, si ana dɔlélea nanyra ɖe edzi.
Le wo katã me la, nu vovovo siwo naa ame ƒe susu me gblẽna vivivi kple ŋkuɖoɖo nu dzi ɖena kpɔtɔna si nye nu si ɖea dzesi le dɔlélea ŋu la ƒe dɔwɔwɔ ɖekae nana woxɔa Alzheimer ƒe dɔlélea.
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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.
Schindler SE, McConathy J, Ances BM, Diamond MI: Advances in diagnostic testing for Alzheimer disease. Mo Med. , 110 (5): 401-5.
Singh VK: Immune-activation model in Alzheimer disease. Mol Chem Neuropathol. , 28 (1-3): 105-11.
['Mɔxeɖenu: atikewɔwɔ']
['Taɖodzinu siwo nye nufiafia kple nyatakaka koe le nyatakakadzraɖoƒe sia ŋu eye menye atikewɔwɔ ŋuti ɖaŋuɖoɖo alo dɔwɔnawo ƒe nya gblɔm wole o.']
['Mele be woazã nyatakaka siwo wona la atsɔ ada dɔléle alo dɔ aɖe o, eye ele be amesiwo di be yewoakpɔ atikewɔwɔ ŋuti ɖaŋuɖoɖo na yewo la nabia ɖɔkta si xɔ mɔɖegbalẽ.']
['De dzesii be neural network si wɔa nyabiabiawo ƒe ŋuɖoɖowo la meɖia o vevietɔ ne wotsɔ xexlẽdzesiwo wɔe. Le kpɔɖeŋu me, ne wotsɔ ame siwo ŋu dɔléle aɖe le ƒe xexlẽme wɔ dɔe.']
['Bia wò ɖɔkta alo lãmesẽdɔwɔla bubu si dze ƒe aɖaŋuɖoɖo ɣesiaɣi le lãmesẽkuxi aɖe ŋu. Mègaŋe aɖaba ƒu aɖaŋuɖoɖo si ɖɔktawo ɖo na wò alo gbɔ dzi ɖi le exexlẽ me le nyatakakadzraɖoƒe sia ta o. Ne èsusu be ɖewohĩ lãmesẽkuxi aɖe le fu ɖem na ye la, ke yɔ 911 alo yi ɖe afisi wokpɔa nɔnɔme kpatawo gbɔ le.']
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['DMCA bia be nàŋlɔ nyatakaka siwo gbɔna ɖe wò nyatakaka si nèŋlɔ be woada le copyright dzi la me: (1) nuŋɔŋlɔ si fia be copyright le dɔ si ŋu wole nu ƒom le la ŋu; (2) nyatakaka si fia be nuŋɔŋlɔa le eme eye wòade mía nu be míake ɖe eŋu; (3) nyatakaka siwo ana míake ɖe ŋuwò, siwo dometɔ aɖewoe nye wò adrɛs, kaƒodzesi kple e-mail adrɛs; (4) wò nya si fia be èxɔe se kple kakaɖedzi be copyright ƒe ame si tɔe nyatakakaa nye, alo eƒe dɔtɔ, alo se aɖeke meɖe mɔ ɖe eŋu o; ']
['(5) Wò ŋutɔ nàŋlɔ agbalẽ si dzi nàde asii, si me nàde se be ne mèwɔe o la, àda alakpa, atsɔ aɖo kpe edzi be nyatakaka siwo le nyatakakaa me la de pɛpɛpɛ eye be ŋusẽ le asiwò be nàʋli agbalẽ siwo ŋu wogblɔ le be woda le la ta.']
['Eye (6) ame si tɔe agbalẽa nye alo ame si wona ŋusẽe be wòawɔ dɔ le ame si tɔ ŋkɔ me la ƒe asinuŋɔŋlɔ alo eƒe asinuŋɔŋlɔ si le mɔ̃ dzi. ']
['Ne mèŋlɔ nyatakaka siwo katã le etame ɖe agbalẽa me o la, ate ŋu ana be wò nyatoƒoe me dzodzro natsi megbe.']
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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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