Vuvabyi bya Alzheimer (AD) i fambiselo ro rharhangana leri katsaka ku hlengeletiwa ka tiphroteyini leti nga tolovelekangiki, ku pfimba ni ku nga tirhi kahle ka tisele ta misiha.
Swikombiso swimbirhi leswikulu swa vuvabyi bya Alzheimer i ku va ni ti-amyloid-beta (Aβ) plaques ni ti-neurofibrillary tangles (NFT) ebyongweni.
Amyloid-beta plaques yi vumbiwa loko swiphemu swa amyloid precursor protein (APP) swi pandziwa hi ti-enzyme leswaku swi vumba ti-Aβ peptides.
Ti-peptide leti ti hlangana kutani ti endla ti-fibril leti nga n'okiki leti hlengeletanaka ehandle ka tisele ta byongo, ti kavanyeta ndlela leyi tisele ti vulavurisanaka ha yona kutani ti endla leswaku tisele ta byongo ti fa.
Ku hlengeletiwa ka ti-Aβ plaque ku tekiwa ku ri xin'wana xa swiendlakalo swo sungula swa ku sungula ka vuvabyi bya Alzheimer naswona ku tekiwa ku ri kona ku vangaka ku tsana ka fambiselo ra misiha.
Ti-neurofibrillary tangles ti vumbiwa loko tiphroteyini ta tau ti va ni ti-phosphorylated to tala kutani ti endla ti-filament leti nga tolovelekangiki endzeni ka tisele ta misiha.
Swiphemu leswi swi kavanyeta matirhelo ya ti-microtubule, leti nga ta nkoka eku fambiseni ka swiaka-miri ni swilo swin'wana endzeni ka tisele ta byongo.
Eku heteleleni, ku hlangana loku ku endla leswaku tisele leti khumbekeke ti fa.
Xitekela xa miri xi hlamula ku hlengeletiwa ka ti-Aβ plaques na NFTs hi ku humesa ti-cytokine leti vangaka ku pfimba, leti nga nyanyisaka ku onhaka ka tisele ta misiha.
Ku engetela kwalaho, ku ni vumbhoni bya leswaku ntshikilelo wa ku gayela, ku nga tirhi kahle ka ti-mitochondrial ni ku kavanyetiwa ka ku gayela ka chukele swi hoxa xandla eka vuvabyi bya Alzheimer.
Swilo leswi swi nga endla leswaku tisele ta misiha ti nga ha tirhi kahle ni ku dlaya, leswi endlaka leswaku vuvabyi byi nyanya.
Hi ku angarhela, vuvabyi bya Alzheimer byi vangiwa hi swilo swo tala leswi endlaka leswaku munhu a nga ha koti ku endla swilo swo karhi ni ku rivala swilo leswi a swi endleke.
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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.
['Xihlambanyo xa vutihlamuleri: swa vutshunguri']
['Website leyi yi endleriwe ku dyondzisa ni ku nyika rungula ntsena naswona a yi nyiki switsundzuxo swa vutshunguri kumbe mintirho ya vativi va swa vutshunguri.']
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['Loko u nga nghenisi vuxokoxoko hinkwabyo lebyi nga laha henhla swi nga endla leswaku ku tirhana ni xivilelo xa wena swi hlwela.']
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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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