Tuwo mar Alzheimer's disease (AD) en tuwo ma kelo tuoche mang'eny moriwo kaka ng'injo mag protein bedo mang'eny, tuoche mag ng'ol, kod tuoche mag obwongo.
Ranyisi ariyo madongo mag AD gin kaka nitie plaques mag amyloid-beta (Aβ) kod neurofibrillary tangles (NFTs) e obwongo.
Amyloid-beta plaques bedoe sama ng'injo mag amyloid precursor protein (APP) ipogo gi enzymes mondo gilos Aβ peptides.
Peptides-go chokore kendo giloso fibril ma ok nyal yudi ma chokore oko mar neuron, kendo mano ketho tudruok e kind ng'injo gi ng'injo kendo miyo ng'injo tho.
Paro ni choko Aβ plaques en achiel kuom gik ma timore chon ahinya e dongruok mar AD, kendo iparo ni okonyo e dongruok mar obwongo.
Neurofibrillary tangles bedoe sama protein tau bedo gi hyperphosphorylated kendo loso filaments ma ok kare ei neuron.
Ng'injo ma kamago ketho yo ma microtubules tiyo godo, ma gin gik madwarore ahinya e ting'o chiemo koda gik mamoko ei neuron.
Gikone, obwongogo miyo ng'injo mag obwongo ma nigi tuwo mar obwongo tho.
Tuwo bende en achiel kuom gik makelo tuwo mar Alzheimer.
Ng'injo mar immunity chiwo dwoko ne Aβ plaques kod NFTs kuom golo pro-inflammatory cytokines, ma nyalo medo hinyruok mar neurons.
E wi mano, nitie gik manyiso ni oxidative stress, mitochondrial dysfunction, kod impaired glucose metabolism konyo e miyo AD obed gi tuwo mar pathophysiology.
Gik ma kamago nyalo miyo ng'ato obed gi tuwo mar obwongo ma ok ti maber kendo mano nyalo miyo otho, kendo mano nyalo miyo tuwo omed bedo marach moloyo.
E yo machuok, tuwo mar Alzheimer nigi gik mang'eny mopogore opogore mamiyo ng'ato bedo gi nyalo mar ng'eyo gik moko e yo maber, kendo mano miyo ng'ato bedo gi paro ma ok kare.
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Whitehouse PJ, Hedreen JC, White CL, Price DL: Basal forebrain neurons in the dementia of Parkinson disease. Ann Neurol. 1983, 13 (3): 243-8.
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.
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.
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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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