Akpáxwé nǔ nɔ jɛ ɖò lanmɛ nɔ ganji hwenu è nɔ jɛ azɔn Alzheimer tɔn é nɔ vɛwǔ tawun, bɔ nǔ enɛ lɛ wɛ nyí ɖɔ nǔkwín e nɔ zɔ́n bɔ è nɔ ɖó wǔvɛ́ lɛ é nɔ jɛji, lanmɛ nɔ jɛ winnya jí, bɔ nǔkwín enɛ lɛ nɔ zɔ́n bɔ nǔ nɔ wà dó lanmɛ nú mɛ wu ɖò nǔwukpikpé tɔn lɛ mɛ ǎ.
Wuntun taji wè e nɔ xlɛ́ ɖɔ azɔnkwín Alzheimer tíìn lɛ é wɛ nyí nǔ e nɔ nyí amyloid-beta (Aβ) bɔ è nɔ ylɔ ɖɔ plaques é kpo nǔ e nɔ nyí neurofibrillary tangles (NFT) bɔ è nɔ ylɔ ɖɔ neurofibrillary tangles é kpo ɖò ta.
È nɔ bló amyloid-beta plaques hwenu e è nɔ wlan nǔ dó amyloid precursor protein (APP) lɛ mɛ gbɔn enzymes lɛ gblamɛ bo nɔ bló Aβ peptides lɛ é.
Peptide enɛ lɛ nɔ kplé bo nɔ bló nǔ kpɛví kpɛví e è ma sixu ɖí xwi xá ǎ lɛ é bɔ ye nɔ kplé ɖò nǔ ɖěɖee nɔ wà nǔ dó lanmɛ nú mɛ lɛ é sín akpa lɛ jí, bo nɔ hɛn nǔ e nɔ wà nǔ dó lanmɛ nú mɛ lɛ é gblé, bɔ nǔ enɛ nɔ zɔ́n bɔ nǔ enɛ lɛ nɔ kú.
È lin ɖɔ nǔ e nɔ jɛ hwɛ̌ ɖò hwenu e azɔnkwín Alzheimer nɔ bɛ́ é mɛ é ɖokpo wɛ nyí nǔ e nɔ zɔ́n bɔ nǔ lɛ nɔ gblé ɖò lanmɛ nú mɛ é.
Neurofibrillary tangles nɔ tɔ́n hwenu e protein tau nɔ ɖó hyperphosphorylated bo nɔ tɔ́n fílamɛnt e ma sɔgbe ǎ lɛ é ɖò nǔ lɛ mɛ é.
Tuto enɛ lɛ nɔ hɛn azɔ̌wiwa nǔ kpɛví kpɛví e nɔ nyí microtubules lɛ é gblé, ɖó ye ɖò taji tawun bo nɔ hɛn nùɖuɖu kpo nǔ ɖevo lɛ kpo yì lanmɛ.
Gudo mɛ ɔ, nǔ e nɔ dɔn nǔ lɛ yì é wɛ nyí ɖɔ nǔ enɛ lɛ nɔ dɔn nǔ ɖěɖee ɖò nǔ wà wɛ lɛ é bǐ yì kú.
E nɔ bló bɔ lanmɛ nɔ cyɔ́n alɔ mɛ nú mɛ é nɔ yí gbè nú nǔ e nɔ kplé ɖò nǔ e nɔ nyí Aβ é kpo nǔ e nɔ nyí NFT lɛ é kpo gbɔn cytocine e nɔ zɔ́n bɔ lanmɛ nɔ syɔ́ lɛ é sín sìn e nɔ tɔ́n é jí, bɔ enɛ sixu zɔ́n bɔ nǔ e nɔ wà nǔ dó wǔjɔnú agbaza tɔn lɛ wu é nɔ syɔ́ d'eji.
Gɔ́ na ɔ, kúnnuɖenú ɖé lɛ xlɛ́ ɖɔ adohu adohu e nɔ zɔ́n bɔ nǔ nɔ ɖyɔ ɖò agbaza mɛ é, nǔ nɔ wà nǔ nyì dò ɖò mitochondrial lɛ mɛ, kpo nǔ nɔ wà nǔ nyì dò nú glucose zinzan kpo nɔ zɔ́n bɔ azɔn nɔ hu mɛ ɖò Alzheimer sín azɔnkwín ɔ hwenu.
Nǔ enɛ lɛ sixu zɔ́n bɔ nǔwukpikpé taglomɛ tɔn lɛ na vɔ bo kú, bɔ azɔn ɔ na syɛn d'eji.
Ðò kplékplé mɛ ɔ, nǔ e nɔ zɔ́n bɔ azɔn Alzheimer nɔ hu mɛ lɛ é sukpɔ́, bɔ nǔ gègě ɖò nǔ wà ɖó kpɔ́ wɛ, bɔ enɛ nɔ wá zɔ́n bɔ nǔwukpikpé nǔwukpikpé tɔn lɛ nɔ ɖekpo kpɛɖé kpɛɖé, bɔ nǔ nɔ bú ɖò ayi mɛ, bɔ azɔn ɔ sín wuntun wɛ.
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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.
['Nǔgbɛnúmɛ: dotóoxwé sín']
['Nǔkplɔnkplɔn kpo nǔsisɔ kpo sín azɔ̌ kɛɖɛ wɛ è nɔ wà dó tɛn ɛntɛnɛti tɔn elɔ jí, bo nɔ na wěɖexámɛ dotóoxwé tɔn alǒ azɔ̌ ɖevo lɛ mɛ ǎ.']
['È ɖó na zán nǔ e è kplɔ́n mɛ lɛ é dó ba azɔn ɖé alǒ azɔn ɖé sín wuntun alǒ dó gbɔ na ǎ, bɔ mɛ ɖěɖee jló na ba wěɖexámɛ dotóo tɔn lɛ é ɖó na yì mɔ dotóo e ɖó acɛ bo nɔ wà azɔ̌ ɖò dotóoxwé é ɖé.']
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["Enyi a ɖi nǔ ɖɔ nǔ ɖĕbǔ ɖò tɛn ɛntɛnɛti tɔn mǐtɔn jí alǒ azɔ̌wiwa mǐtɔn lɛ jí bo hɛn nǔ dó así nú mɛ ɔ, é xò nǔ dó acɛ nǔɖògbɛ́ towe lɛ wu ɔ, hwi (alǒ mɛ e nɔ kpé nukún dó wǔ towe é) sixu sɛ́ wɛn dó mǐ, bo byɔ ɖɔ mǐ ni ɖè nǔ ɖ'emɛ lɛ sín tɛn ɔ jí, alǒ ɖɔ mǐ ni sú ali dó mɛ."]
["È ɖó ná sɛ́ mɛ dó gbɔn email jí (e-mail è nɔ dó ɔ́' kpɔ́n 'Kɔntaktɔ́' ɔ́)."]
['DMCA byɔ ɖɔ ɖɔ nǔ elɔ lɛ ni nɔ akpáxwé nǔ e a ɖɔ é gbà acɛ dó nǔ é tɔn jí é: (1) xó dó azɔ̌ e ɖó acɛ dó nǔ é jí; (2) xó dó nǔ e ɖó acɛ dó nǔ é jí, kpo nǔ ɖevo e na zɔ́n bɔ mǐ na mɔ nǔ ɔ lɛ é kpo; (3) xó dó hwiɖée wu, ɖi adlɛsi towe, alokan towe kpo email towe kpo; (4) xó ɖɔ dó nǔ e wu a ɖi nǔ ɖɔ nǔ e ɖó acɛ dó nǔ e jí a ɖɔ é jí é kún nyí nǔ e ɖó acɛ dó nǔ é jí tɔn ɔ, alǒ mɛ e nɔ kpé nukún dó nǔ é tɔn wu é sín acɛ ó; ']
["(5) Ðɛ́ mɛ̀ è mi sɔ́ alɔ dó ɖ'así ná ɖò hwɛɖɔxɔsá ɔ́' è ɖó ná ɖó hwɛ̀ ɖɔ̀ xó è mi ɖɔ ɖò mɛ̀ è mi dó wèmá ɔ́ mɛ̀ ɔ́' sɔgbe bɔ̀ mi ɖó acɛ̀ bó ná dó ba ɖɔ è ní sú nǔ è è dó wèmá ɔ́ wú lɛ́ɛ sín axɔ́."]
['bɔ (6) alɔ wlanwlan mɛ e ɖó acɛ dó nǔ é tɔn alǒ mɛ e ɖó acɛ bo na wà nǔ dó wutu tɔn é tɔn. ']
['Nú a ma gɔ́ nǔ e ɖò jí lɛ é bǐ ǎ ɔ, é sixu zɔ́n bɔ è na lín có bo na dóhwɛ we.']
['Wǎ kpé mì']
['Mi kɛnklɛn bo sɛ́ nǔkanbyɔ mitɔn lɛ dó mǐ gbɔn e-mail jí.']
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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