Say pathophysiology na Alzheimer's disease (AD) et komplikadon proseso a mangilalanor ed pakatipon na saray abnormal a protina, pamamaga, tan pakaka-disfunction na neuron.
Say duaran manunan pakabidbiran ed Alzheimer's et say presensia na amyloid-beta (Aβ) plaques tan neurofibrillary tangles (NFTs) diad utek.
Nabuo iray beta-amyloid plaque sano saray fragments na amyloid precursor protein (APP) et napultot na saray enzyme pian magmaliw ya Aβ peptide.
Sarayan peptide et mantitipon tan manggaway fibril ya agnatunaw tan mantitipon ed paway na neuron, kanian naderal so komunikasyon na selula tan ompatey so neuron.
Say pantipon na Aβ plaques so ipapasen a sakey ed saray sankaunaan a nagagawa ed pakawalaay AD, tan panisiaan a makatulong itan ed proseso na neurodegenerative.
Nabuo iray neurofibrillary tangles sano say protein a tau et magmaliw ya hyperphosphorylated tan mamawala na abnormal iran filaments ed loob na saray neuron.
Sarayan patit et makaderal ed normal ya ikukurang na saray microtubule, ya importante ed pangiyalis na sustansia tan arum nin materyal diad loob na neuron.
Say pansasabit na saratan so manresulta ed ipatey na saray apektadon neuron.
Wala met so betang na inflammation ed pathophysiology na Alzheimer's.
Say immune system et onebat ed pantipon na Aβ plaques tan NFTs diad pangipaway na pro-inflammatory cytokines, ya nayarin mamaloor ed pakaderal na neurons.
Niarum ni, wala ray ebidensya a say oxidative stress, mitochondrial dysfunction, tan impaired glucose metabolism so sengegan na Alzheimer's.
Sarayan sengegan so nayarin manresulta ed pakapuyan tan ipatey na saray neuron, a lalon mamaloor ed sakit.
Diad inkalapagan, say pathophysiology na Alzheimer et komplikadon pantutulongan na dakel iran sengegan a manresulta ed kalkalnan ikakapuy na kognitibo tan pakaandi na memorya a pakapatnagan na sakit.
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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.
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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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