What is pathophysiology of Alzheimer?

['Thikĩrĩria karatathi gaka']

Mũrimũ wa Alzheimer's ũtariĩ atĩa?

Mũrimũ wa Alzheimer's (AD) nĩ mũrimũ wa meciria ũrĩa ũrehaga mĩrimũ ĩngĩ ta mũrimũ wa gũkua ciĩga (neurons).

Maũndũ merĩ marĩa monanagia mũrimũ wa Alzheimer nĩ ta mũrimũ wa tũcunjĩ twa proteini twĩtagwo beta-amyloid (Aβ) na tũcunjĩ tũngĩ tũtagwo neurofibrillary tangles (NFT) thĩinĩ wa tombo.

Tũcunjĩ twa proteini ĩtagwo amyloid precursor protein (APP) nĩ tũthondekagwo nĩ enzymes nĩguo ithondeke tũcunjĩ twa proteini ĩtagwo Aβ.

Tũcunjĩ tũu twa proteins twĩthondekagĩra tũcunjĩ tũngĩ tũtangĩnyitanĩra na tũngĩ tũthondekwo na njĩra ĩngĩ. Tũcunjĩ tũu twa proteins tũthondekagwo na njĩra ĩngĩ tũthondekagwo na njĩra ĩngĩ.

Kũingĩha kwa tũcunjĩ twa Aβ gũkoragwo kũrĩ ũndũ ũmwe wa mbere harĩ gũthondekwo kwa mũrimũ wa AD, na nĩ kũrehaga gũthũka kwa tombo.

Neurofibrillary tangles ciũmbagwo rĩrĩa proteini ya tau yagĩa na phosphorylated mũno na ĩgathondeka tũcunjĩ tũtarĩ twa ndũire thĩinĩ wa tũcunjĩ twa tombo.

Tũcunjĩ tũu tũthũkĩtie wĩra wa tũcunjĩ tũu tũnini tũrĩa tũbataranagia harĩ gũtwara irio na indo ingĩ thĩinĩ wa kahengereta.

Macũngĩrĩro-inĩ, tũhengereta tũu tũkuaga.

Mũrimũ wa kũimba ũkoragwo na itemi harĩ gũthondeka mũrimũ wa mũrimũ wa AD.

Ciĩga cia mwĩrĩ iria irũaga igũaga harĩ kũingĩha kwa tũcunjĩ twa Aβ na NFTs na njĩra ya kũruta tũcunjĩ twa cytokine, tũrĩa tũngĩthũkia makĩria neurons.

Makĩria ma ũguo, kũrĩ ũira wonanagia atĩ mũrimũ wa mũrimũ wa Alzheimer's ũtambĩte kũhonio nĩ ũndũ wa kũhũyũka kwa indo ta thakame, gũthũka kwa mitochondrial, na kwaga gũkinyanĩra kwa glucose.

Maũndũ macio no matũme tombo ũremwo nĩ kũruta wĩra wega na ũkue, na ũndũ ũcio no ũtũme mũrimũ ũthire na mbere.

Ũndũ ũmwe nĩ atĩ, mũrimũ wa Alzheimer ũrehaga maũndũ maingĩ marĩa macokaga magatũma mũndũ ambĩrĩrie kũgĩa na mathĩna ma meciria na kũriganĩrũo.

['Ũhoro wa kwambĩrĩria']

PubMed/Medline https://www.nlm.nih.gov/databases/download/pubmed_medline.html

RefinedWeb https://arxiv.org/abs/2306.01116

Nemeroff CB: The preeminent role of neuropeptide systems in the early pathophysiology of Alzheimer disease: up with corticotropin-releasing factor, down with acetylcholine. Arch Gen Psychiatry. 1999, 56 (11): 991-2.

Skoog I, Kalaria RN, Breteler MM: Vascular factors and Alzheimer disease. Alzheimer Dis Assoc Disord. , 13 Suppl 3 (): S106-14.

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.

Raskind MA, Peskind ER: Neurobiologic bases of noncognitive behavioral problems in Alzheimer disease. Alzheimer Dis Assoc Disord. 1994, 8 Suppl 3 (): 54-60.

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.

['Ũkaana: thibitarĩ']

['Website ĩno ĩkoragwo ĩrĩ ya kũrutana na kũheana ũhoro tu na ti ya kũheana ũtaaro wa ũrigitani kana ũtungata wa kĩĩmwĩrĩ.']

['Ũhoro ũrĩa ũrĩ thĩinĩ wa broshua ĩyo ndwagĩrĩirũo kũhũthĩrũo gũthima kana kũrigita mũrimũ mũna, na arĩa marenda ũtaaro wa ũrigitani magĩrĩirũo gũcaria ũteithio wa ndagĩtarĩ.']

['No wone atĩ netiwaki ya neuron ĩrĩa ĩheanaga macokio ma ciũria icio, ndĩkoragwo na ũkinyanĩru mũno ũhoro-inĩ wĩgiĩ namba. Kwa ngerekano, mũigana wa andũ arĩa magwatĩtio mũrimũ mũna.']

['Hingo ciothe caria ũtaaro wa ndagĩtarĩ kana mũndũ ũngĩ wagĩrĩire ũgima-inĩ waku wa mwĩrĩ igũrũ rĩgiĩ mũrimũ. Ndũkaanahũthie ũtaaro wa ndagĩtarĩ kana ũcererũo kũũcaria nĩ ũndũ wa ũndũ ũthomete thĩinĩ wa website ĩno. Ũngĩkorũo ũrona ta wacemania na ũndũ mũhiũ, hũra thimũ 911 kana ũthiĩ thibitarĩ ya hakuhĩ na harĩa ũrĩ. Gũtirĩ ũrata wa ndagĩtarĩ na mũrwaru wonekaga nĩ ũndũ wa website ĩno kana kũhũthĩrũo kwayo. BioMedLib kana aruti ayo a wĩra, kana mũndũ ũngĩ wothe ũrutĩte wĩra thĩinĩ wa website ĩno, ndarĩ na ũira, wa ĩmwe kwa ĩmwe kana wa ĩmwe kwa ĩmwe, wĩgiĩ ũhoro ũrĩa ũheanĩtwo ho kana ũrĩa ũhũthĩrĩtwo.']

['Ũregani: wĩyathi wa kwandĩka']

['Watho wa Digital Millennium Copyright Act wa 1998, 17 U.S.C. § 512 (the DMCA) ũheanaga ũhoti wa ene a ihoto cia wandĩki arĩa metĩkĩtie atĩ ũhoro ũrĩa ũroneka intanetiinĩ nĩ ũtharĩtie ihooto ciao kũringana na watho wa U.S. wa ihoto cia wandĩki.']

['Ũngĩkorũo na wĩtĩkio atĩ ũhoro kana kĩndũ kĩna gĩtahingũrĩtwo ũhoro-inĩ wĩgiĩ website kana ũtungata witũ nĩ gĩgũthũkia ihooto ciaku, wee (kana mũndũ ũrĩa ũgũgũthondekera) no ũtũtũmĩre notithi ũkĩũria ũhoro kana kĩndũ kĩu kĩeherio, kana ũrigĩrĩrio ndũgacihũthĩre.']

["Marũa macio magĩrĩire gũtũmwo na njĩra ya kwandĩkwo na e-mail (rora ũhoro wa andirethi gĩcunjĩinĩ kĩa 'Maũndũ ma kwaranĩria')."]

['DMCA ĩbataraga atĩ notithi yaku ya kuuna ihooto cia wandĩki ĩkorwo na ũhoro ũyũ: (1) ũtaarĩria wa wĩra ũrĩa ũrĩ na ihooto cia wandĩki ũrĩa ũrarumwo; (2) ũtaarĩria wa ũhoro ũrĩa ũrarumwo na ũhoro mũiganu wa gũtũhotithia kũmenya kũrĩa ũhoro ũcio ũrĩ; (3) ũhoro waku wa kwaranĩria, hamwe na andirethi, namba ya thimũ na andirethi ya e-mail; (4) ndũmĩrĩri yaku atĩ wĩ na wĩtĩkio mwega atĩ ũhoro ũcio ũramenererio ndũrĩ na rũtha rwa mwene wa watho, kana mũrũgamĩrĩri, kana rwa watho o wothe; ']

['(5) nĩ mwandĩkanĩire, na nĩ mũkũheo mũkaana wa kũheenania, atĩ ũhoro ũrĩa ũrĩ kĩmenyithiainĩ kĩu nĩ wa ma na atĩ mũrĩ na ũhoti wa kũhingia ihooto iria mũreganĩte nacio;']

['na (6) kĩrore kĩa mwene kĩhoto kana kĩa mũndũ wĩtĩkĩritio gwĩtongoria handũ ha mwene kĩhoto.']

['Kwaga kwandĩka ũhoro ũcio wothe no gũtũme gũtangĩka gwaku kũhĩtũke.']

['Ũhoro wa Kwaranĩria']

['Tũma ndũmĩrĩri ya kũbucia kũgerera thimũ kana thimũ ya mohoro.']

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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