O uhaxi ua uongo (Alzheimer) u bhangesa o uongo ku kamba ku kalakala kiambote.
O uhaxi ua Alzheimer u tu londekesa kuila, o uongo uetu uala ni ijimbuete iiadi - o ijimbuete ia beta-amyloid (Aβ) ni ijimbuete ia neurofibrillary tangles (NFT).
O uhaxi iú, a uixana anemia beta-amyloid, mukonda o ima ia beta-o-kota ku muenhu, o ima ia kate.
O ji célula jiji, ji di bunda ni ku bhanga mbandu ku mukutu ua muthu, phala ku kala ni nguzu ia ku bhanga o ima.
O uhaxi iú ua beta ku kala ni valolo ku mukutu ua muthu, mukonda u bhangesa o uongo ku kamba ku kalakala kiambote.
O ji neuron ji kala ni ji fibrila javulu, kioso o proteína tau ki i kala ni nguzu iavulu, o ji fibrila ji kituka ja iibha.
O ji célula jiji, ji fidisa o ji microtubules ku kalakala kiambote, phala o ji neurónios ji tene kuambata o kudia ni ima ia mukuá.
O ji célula jiji, ji fuá.
O uhaxi ua kukohona ua dibhute ué.
O ji célula ji zokela ni ji célula ja mukuá, ji kuatekesa o mukutu ku di langa ku mauhaxi.
Mu kifika, o uhaxi ua dibhute, u bhangesa o muthu ku kala ni njinda iavulu.
O ima íii i tena ku bhangesa o uongo ku kamba ku kalakala kiambote, ni ku bhangesa o uongo ku kamba ku kalakala kiambote.
O uhaxi ua Alzheimer u bhangesa o muthu ku jimba o ima ni ku kamba kilunji.
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.
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.
['Kitendelesu:']
['O kijimbuete kiki, phala ku longa ngó, ki kiene mu bhana milongi ia lungu ni sauidi.']
['O milongi íii, ka tokala ku i tumbula phala ku saka uhaxi, mba ku saka mauhaxi a mukuá.']
['Mu kifika, o ji komputadolo jene mu kuatekesa o athu kuijiia o ima ia lungu ni uhaxi, ki ji tena ku jimbulula kiambote o maka.']
['Sota kikuatekesu kia dotolo iê mba muthu ua mukuá uala ni uhete ua ku saka mauhaxi. Kana ku jimba o itendelesu ia dotolo mukonda dia milongi i ua tange mu kijimbuete kiki. Se ua mesena kikuatekesu, xinda ku muxinda ua 112, mba ndé mu inzo ia ku saka ia zukama.']
['Iala ni Kikutu ni Jinguvulu ja Jixi Jengi']
['O Digital Millennium Copyright Act of 1998, 17 U.S.C. § 512 (o DMCA) i bhana ku athu ala ni ufolo ua ku soneka, o ima ia mona mu Internete, i bhukumukina o ufolo uâ ua ku soneka. ']
['Se eie u xikina ni kidi kioso kuila o milongi mba milongi i ua mu tanga mu kijimbuete kietu kia internete, mba mu ima ia mukuá, ia mu bhukumukina o itumu iê, eie (mba o muthu u ua mu tumina) u tena ku tu tumikisa mukanda ni ku tu bhinga phala ku katula o milongi mba milongi i ua mu tanga mba ku fidisa o muthu ku i tanga.']
['O ngolokela a tokala ku i tumikisa mu mukanda ni mu kijimbuete kia i-me-le (Tala o mbandu "Utuameni ua Ijimbuete") ].']
['O DMCA i bhinga kuila o njimbu iê ia lungu ni ku bhukumukina o itumu ia ku tokala, i kala ni milongi íii: (1) kijimbuluilu kia kikalakalu kia tokala ku kitumu kia ku tokala; (2) kijimbuluilu kia milongi ia ku tokala ni milongi i tua tokala ku sanga; (3) o ijimbuete iê, ni ijimbuete ia mutelembe uê; (4) ni izuelu i ua zuela kuila eie u xikina ni kidi kioso kuila o milongi ia ku tokala, ki i tokala ku ngana ia tokala, mba ku mukunji uê, mba ku kitumu kioso-kioso; ']
['(5) O kijimbuete kiê, ni kijimbuete kia ku tangela kuila o milongi iala mu kijimbuete kiki ia kidi, ni kuila eie uala ni kutena kua ku langa o ima ia ku tokala;']
['O kijimbuete kiki, ki tena ku kala ni kidimbu kiê, mba kijimbuete kia muthu ua mu tumina o ku ki jikula.']
['Se ku soneka o ima ioso íii, o ku tokuesa o maka mê kua-nda laleka.']
['Kuzuela ni Muthu']
['Tua ku dióndo, tu tumikise njimbu ni ibhuidisu mba jindunge.']
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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