Isifo se-Alzheimer isifo esiyingozi esibuchosheni. Ukuqonda ukuthi isimo se-Alzheimer's ihluke kanjani ebuchosheni obuvamile sisenza siqonde. Kungasisiza ukuba sibhekane kangcono nezinguquko ezenzeka kubathandekayo bethu ngenxa yalesi sifo esilimazayo.
E- Alzheimer's disease , ukubonakala kobuchopho obuthintekile ku-Alzheimer kuhluke kakhulu ebuchosheni obuvamile.
I-cerebral cortex atrophies. Lokhu kusho ukuthi le ndawo yobuchopho iyancipha futhi le shrinkage ihluke ngokuphawulekayo kwi-cortex ye-cerebral yobuchopho obuvamile. I-cortex ye-cerebral yindawo engaphandle yengqondo. Kuphethwe wonke ukusebenza kwengqondo. Kunezinguquko ezimbili ezinkulu ezingabonwa ebuchosheni be-autopsy:
- Inani lempilo ebuchosheni bobuchopho (i-gyri) liyancipha
- Izikhala ezinhlangothini zobuchopho (i-sulci) zanda kakhulu.
Okuncane kakhulu kunezinguquko eziningana ebuchosheni futhi.
Iziphumo ezimbili ezibalulekile ebuchosheni buka-Alzheimer ziyi- amyloid plaques kanye ne-neurofibrillary tangles. Amapulangwe angama-Amyloid atholakala ngaphandle kwe-neurons, ama-plaque e-neurofibrillary atholakala ngaphakathi kwe-neurons. Ama-neurons angama-cell nerve ngaphakathi kwengqondo.
Ama-plaques namathangathi atholakala ebuchosini babantu abangenawo i-Alzheimer's. Yizibalo eziningi zazo eziphawulekayo esifweni se-Alzheimer's.
Umsebenzi we-Amyloid Plaques
Amapulangwe angama-Amyloid amaningi akhiwa amaprotheni okuthiwa i-B-amyloid amaprotheni okuyiyona eyingxenye yeprotheni elikhulu kakhulu elibizwa nge-APP (i-amyloid precursor protein). Lezi yi-amino acid.
Asazi ukuthi i-APP iyini. Kodwa siyazi ukuthi i-APP yenziwe esitokisini, ithuthelwa embranini yeseli futhi kamuva ihlehlisiwe.
Izindlela ezimbili ezibalulekile zihileleka ekwehleni kwe-APP (amyloid precurrent protein). Indlela eyodwa evamile futhi ayibangeli inkinga. Owesibili kubangelwa izinguquko ezitholakala ku-Alzheimer nakweminye iminye imimoya.
Ukuphazamiseka Kwendlela Eholela Ekulimaleni Kwe-Alzheimer
Esikhathini sesibili sokuphutha i-APP ihlukaniswa yi-enzymes B-secretase (B = beta) bese y-secretase (y = gamma). Ezinye zezingcezu (ezibizwa ngama-peptide) ezitholela ndawonye futhi zakha uchungechunge olufushane oluthiwa i-oligomer. Ama-oligomers ayaziwa nangokuthi i-ADDL, ama-diffusible ligands athola ama-amyloid-beta. Ama-oligomers we-amyloid beta 42 abonisiwe abangela izinkinga ekukhulumisaneni phakathi kwe-neurons. I-beta ye-Amyloid 42 nayo iveza izintambo ezincane, noma ama-fibrils. Uma bebamba ndawonye benza i-amyloid plaque. Ezinye zalezi zigcawu zingazifaka embranini ye-neuron cell edala izinto ezingaphandle kweseli ukuze zigijime kulo, zenze umonakalo owengeziwe. Lo monakalo uholela ekwakheni ama-peptides ama-Amyloid beta 42 aholela ekusebenzeni kwe-neuron nokushona.
Indima Yezingxenyana Ze-Neurofibrillary
Okwesibili okutholwa yi-Alzheimer's brain is a neurofibrillary tangles. Ama-neurofibrillary tangles akhiwa amaprotheni okuthiwa i-tau amaprotheni.
I-tau amaprotheni idlala indima ebalulekile ekusungulweni kwe-neuron. Kubantu abanamaprotheni e-Alzheimer's tau abangela ukungavamile ngokusebenzisa ama-enzyme angasebenzi kakhulu okuholela ekubunjweni kwezingxenyana ze-neurofibrillary. Ama-neurofibrillary tangles abangela ukufa kwamaseli.
Ukufingqa kobuchopho be-Alzheimer's
Indima yama-amyloid plaques kanye ne-neurofibrillary tangles ekusebenzeni kobuchopho akukaze kuqondwe ngokugcwele. Iningi labantu abanesifo se-Alzheimer libonisa ubufakazi bomabili ama-plaque nama-tangles, kodwa inamba encane yabantu abane-plazzi kuphela i-Alzheimer kanti abanye banama-neurofibrillary tangles kuphela.
Abantu abane-plaque kuphela i-Alzheimer's show a slower rate of deterioration ngesikhathi sokuphila kwabo.
Abantu abanezintambo ze-neurofibrillary cishe banokutholwa ukuthi bane- dementia ye-frontotemporal .
Ucwaningo olubhekene nesifo se-Alzheimer luyatholakala ngokuningiliziwe nge-anatomy ne-physiology yobuchopho. Njengoba siqonda kabanzi mayelana nendima yamacwecwe nama-tangles agcinwe ebuchosheni buka-Alzheimer, sisondeza kakhulu ekuphumeleleni okuphawulekayo kanye nokwelashwa kwesifo se-Alzheimer's.