Pathophysiology nyau Alzheimer (AD) lati dabare je ɗon hawta be moftal proteinji je wala no, fuɗɗam, be huudure neuronal.
Mandolji nyau AD ɗiɗi woni wondugo leekuji beta-amyloid (Aβ) be neurofibrillary tangles (NFT) ha nder ngaandi.
Amyloid-beta plaques ɗon waɗa to pecce protein je ɗon aandi be amyloid (APP) ɗon fecca gal enzymes ngam waɗugo Aβ peptides.
Peptideji ndu ɗon hawta e ɗon waɗa fibrils je ɗon mofta ta'irdeji ɓaandu je ɗon mofta yaasi ɓikkoy ɓaandu, ɗon darna bolwugo hakkunde ɓikkoy ɓaandu e ɗon waɗa ɓikkoy ɓaandu maaya.
Hauti be moftal ɓikkoy Aβ lati bana go'oto ha aranol yahde AD, e ɗon bana ɗon waɗa yahde neurodegenerative.
Neurofibrillary tangles ɗon waɗa to protein tau ɗon waɗa hyperphosphorylated e ɗon waɗa filamentji je wala no ha nder neurons.
Kujeji ndu ɗon darna kugal microtubules je ɗon mari haaje ngam yahde kujeji je ɗon nyaɗina be kujeji feere ha nder neuron.
Kujeji je ɗon hawta ɗon waɗa ɓawo man neuronji je ɗon mari nyau maaya.
Wullol ɗon mari bo'o kugal ha nder dabare nyaɗugo AD.
Dabare fadol ɓaandu ɗon no jaabano moftal leekuji Aβ be NFT gal wurtinugo cytokines je ɗon hokka ɓaandu fuɗɗam, je footi ɓesda bone ha nder taklonji.
Fahin bo'o, wodi sappinolji je holli yo'o ɓernde je ɗon mari sembe, kugal mitochondrial je ɗon mari sembe, be kugal glucose je ɗon mari sembe ɗon hokka sababuji nyaɗugo AD.
Ko ɓuri fu, pathophysiology AD lati dabareji jur je ɗon yahida be feere feere je ɗon yahida be ustol yahde kugal andal be majjugo siftorgo je ɗon holla nyau ndu.
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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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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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