Ũwau wa Alzheimer ũtumaa mũndũ ethĩwa na mathĩna meva?
Ũwau wa Alzheimer (AD) nĩ ũwau mũthũku mũno na ũetae mathĩna maingĩ ma mwĩĩ.
Maũndũ elĩ ala matumaa mũndũ ethĩwa na ũwau ũsu nĩ kwĩthĩwa na tũlungu twĩtawa beta-amyloid (Aβ) na tũlungu tũngĩ twĩtawa neurofibrillary tangles (NFT) twĩ mũtwe.
Myakanĩ ya mĩtũkĩ, andũ aingĩ nĩmambĩĩe kũtũmĩa ndawa sya kũmila na sya kũiita.
Syĩndũ isu syĩtawa peptides nitumaa twĩndũ tũnini tũla tũtatonya kũlika nthĩnĩ wa mwĩĩ (insoluble fibrils) twĩthĩwa na vinya wa kũlika nthĩnĩ wa mwĩĩ wa mũndũ. Syĩndũ isu syĩkĩkaa nza wa twĩndũ tũu (neurons) na ũu ũituma twĩndũ tũu tũeka kũea ngewa na tũieka kũkw'a.
Kĩndũ kĩmwe kĩtumaa andũ makwatwa nĩ ũwau ũsu nĩ kwingĩva kwa tũlungu twa Aβ ĩla mũndũ wambĩĩa kũwaa.
Neurofibrillary tangles nĩ myalĩka ĩla yĩthĩawa na protein yĩtawa tau ĩla yĩthĩawa na phosphorylation mbingĩ na ĩituma ĩseũvya tũlungu twĩ kĩvathũkany'o na tũla twĩthĩawa tũseũvĩtye mĩĩ ya andũ.
O na ĩngĩ, ĩla twĩ na tũla twĩndũ tũnini twĩtawa microtubules, nĩtwĩthĩawa na mathĩna maingĩ.
Ĩtina wa ĩvinda, tũsamũ tũu tũnini tũla tũkũaa twĩsaa kũkw'a.
O na ĩngĩ, ũwau ũsu no ũtume mũndũ awaa.
Ĩla mwĩĩ wa mũndũ wambĩĩa kũkita na tũsamũ tũu, mwĩĩ nĩw'o ũmanengae vinya wa kũkita na tũsamũ tũu.
O na ĩngĩ, ve ũkunĩkĩli ũkwonany'a kana mũndũ eethĩwa na ũwau wa Alzheimer, no athĩnw'e nĩ syĩndũ ila syĩthĩawa nthĩnĩ wa mwĩĩ (oxidative stress), na ethĩwa mitochondria ndĩthũkũmaa nesa, na ethĩwa mwĩĩ wake ndwĩsa kũvĩndũa glucose nesa.
Maũndũ asu nĩmatonya kũtuma tũlũkũ tũu tũeka kũthũkũma nesa na tũikw'a, na ũu ũituma ũwau ũendeea na kwingĩva.
Ũwau wa Alzheimer ũtumaa mũndũ ethĩwa na mathĩna maingĩ ma kĩlĩko na ũituma aeka kũlilikana maũndũ ala weekĩte tene.
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.
['Ũtao:']
["Kĩsese kĩĩ kĩseũvĩtw'e kwondũ wa kũmanyĩsya na kũtetheesya andũ, ĩndĩ ti kũnengane motao ma ũiiti kana ũtethyo ũngĩ."]
['Ũvoo ũla wĩ vo ndwaĩle kũtũmĩwa kũĩkĩĩthya kana mũndũ e na ũwau mũna, na ala mekwenda ũtao wa ũiiti maĩle kũneena na ndakĩtalĩ.']
["Kwa ngelekany'o, ĩla mũndũ wakũlya ĩkũlyo yĩ na namba, no amanye kana mũndũ ũsu e na ũwau mũna."]
['Kĩla ĩvinda neena na ndakĩtalĩ waku kana mũndũ ũngĩ ũsomeete maũndũ ma ũiiti. Ndũkaatate kũlea kana kũkua ĩvinda ũimũkũlya ũtao aĩ nũndũ wa maũndũ amwe wasoma Kĩsesenĩ kĩĩ. Ethĩwa wĩona ta wĩ na thĩna wa mĩtũkĩ, neena na namba ya 911 kana ũthi sivitalĩ ya mĩtũkĩ ĩla yĩ vakuvĩ.']
['Ũtao:']
['The Digital Millennium Copyright Act of 1998, 17 U.S.C. § 512 (the DMCA) nĩyaĩtye kana ala me na ũthasyo wa kumĩthya syĩndũ ila syĩ Indanetinĩ nĩmaĩle kũtata ũndũ matonya nĩ kana maĩkĩĩthye kana syĩndũ ila mekumĩthya nĩsyavĩnga mĩao ya nthĩ ya Amelika.']
['Ethĩwa wĩ na mũĩkĩĩo kana ũvoo ũla wĩ kĩsesenĩ kitũ kana nthĩnĩ wa syĩndũ ila tumasya nũvĩtĩsye mĩao yaku, no ũtũtũmĩe valũa ũũtwĩĩte kana no ũtũsiĩĩe tũikamĩsome.']
["Mĩao ya DMCA yaĩtye kana no nginya ũvoo ũla ũũtũmĩa kũtũtavya kana ve kĩndũ kĩna kĩnavĩnga mĩao ya kumĩthya syĩndũ wĩthĩwe na ũvoo ũũ: (1) ũvoo ĩũlũ wa syĩndũ ila iwetetwe kana nĩsyo ivĩngĩĩsiwe nĩ mĩao ĩsu; (2) ũvoo ĩũlũ wa syĩndũ ila iwetetwe kana nĩsyo ivĩngĩĩsiwe nĩ mĩao ĩsu na ũvoo ũtonya kũtũtetheesya kũmanya vala syĩndũ isu syĩ; (3) ũndũ ũtonya kũtũtavya ũndũ ũtonya kũtũtavya ũndũ ũtonya kũũkũlya, ta vala wĩkalaa, namba yaku ya simũ, na valũa waku wa simũ; (4) ũĩkĩĩthyo ũkwonany'a kana wĩ na mũĩkĩĩo kana syĩndũ ila iwetetwe vau iyĩtĩkĩlĩtw'e nĩ ũla wĩ na ũthasyo wa kũseũvya syĩndũ, kana nĩ mũũngamĩi wasyo, kana nĩ mĩao ĩngĩ."]
["(5) ũĩkĩĩthyo kuma kwaku, ũla ũandĩkĩte ũikĩa ũkũsĩ ũte wa w'o, kana ũvoo ũla wĩ nthĩnĩ wa livoti nĩ wa w'o na kana wĩ na ũkũmũ wa kũũngamĩa maũndũ ala mawetwa nĩ ũla ũkũũmĩw'a;"]
['Na (6) saii ya mwene syĩndũ kana mũndũ ũla ũnengetwe ũkũmũ wa kwĩka maũndũ kwondũ wake.']
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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