Ko te pathophysiology o te mate a Alzheimer (AD) he mahinga uaua e uru ana ki te kohinga o nga pūmua koretake, te mumura, me te ngoikoretanga o te neuronal.
Ko nga tohu matua e rua o te AD ko te aroaro o nga papa amyloid-beta (Aβ) me nga tangles neurofibrillary (NFTs) i roto i te roro.
Ka hangaia nga papa amyloid-beta ina pakaru nga kongakonga o te pūmua amyloid (APP) e nga whākōkī hei hanga i nga peptides Aβ.
Ka whakakotahi ēnei peptides, ka hanga i ngā muka kāore e taea te wairewa e kohikohi ana i waho o ngā pūtau, e whakararuraru ana i te whakawhitiwhiti pūtau-ki-pūtau, ā, ka mate ai te pūtau.
Ko te whakahiato i nga papa Aβ e kiia ana ko tetahi o nga huihuinga tuatahi i te whanaketanga o te AD, a e whakapono ana ka uru ki te mahi neurodegenerative.
Ka hangaia nga tangles Neurofibrillary ina riro te pūmua tau hyperphosphorylated ka hanga i nga miro rereke i roto i nga neurons.
Ka whakararuraru ēnei kōpaki i te mahi noa o ngā microtubules, e tino nui ana mō te kawe i ngā matūkai me ētahi atu rauemi i roto i te pūtau.
Ko te mutunga iho ka mate nga pūtau ārai mate.
He wāhi anō tō te mumura ki te pathophysiology o AD.
Ka urupare te pūnaha ārai mate ki te whakahiato o ngā papa Aβ me ngā NFT mā te tuku i ngā pūtau pro-inflammatory, e kaha ake ai te kino ki ngā pūtau.
Hei taapiri, he taunakitanga kei te kaha te ahotea o te waikura, te ngoikoretanga o te mitochondrial, me te ngoikoretanga o te pākia huka e uru ana ki te pathophysiology o AD.
Ka taea e ēnei āhuatanga te arahi ki te ngoikoretanga o te pūtau me te mate, ka kaha ake te tukanga mate.
I te katoa, ko te pathophysiology o te AD he whakawhitinga matatini o nga take maha e arahi ana ki te heke haere o te mahi hinengaro me te ngaro o te mahara e tohu ana i te mate.
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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.
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Singh VK: Immune-activation model in Alzheimer disease. Mol Chem Neuropathol. , 28 (1-3): 105-11.
['Whakakahoretanga: hauora']
['Ko tenei paetukutuku e whakaratohia ana mo nga kaupapa ako me nga korero anake, kaore hoki e whakarato i nga tohutohu hauora, i nga ratonga ngaio ranei.']
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["Me tuku ngā whakamōhiotanga ā-tuhi mā te īmēra (tirohia te wāhanga 'Whakapā' mō te wāhitau īmēra). "]
['E hiahiatia ana e te DMCA kia whakaurua ki tō whakamōhiotanga mō te whakawātea mana pupuri i ngā mōhiohio e whai ake nei: (1) whakaahuatanga o te mahi mana pupuri e pā ana ki te whakawātea e whakapaetia ana; (2) whakaahuatanga o te ihirangi e whakapaetia ana e takahi ana me ngā mōhiohio e tika ana kia taea ai e mātou te kimi i te ihirangi; (3) mōhiohio whakapā mōu, tae atu ki tō wāhitau, tau waea me tō wāhitau īmēra; (4) he tauākī nāu e whakapono pono ana koe kāore te ihirangi i te āhua e amuamutia ana i whakamanahia e te kaipupuri mana pupuri, e tana māngai rānei, e te whakahaerenga rānei o tētahi ture; ']
['(5) he tauākī nāu i haina, i raro i te whiu o te whakapae teka, e tika ana ngā mōhiohio i roto i te whakamōhiotanga, ā, kei a koe te mana ki te whakatinana i ngā mana pupuri e kīia ana kua takahia;']
['me te (6) he waitohu ā-tinana, ā-rorohiko rānei a te kaipupuri mana pupuri, a tētahi tangata rānei kua whakamanahia ki te mahi mō te kaipupuri mana pupuri. ']
['Ki te kore e whakaurua ngā mōhiohio katoa i runga ake nei, ka whakaroa pea te tukatuka o tō amuamu.']
['Whakapā']
['Tena koa tukuna mai he imeera ki a maatau me tetahi patai / whakaaro.']
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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