E fisiopatologia di Alzheimer ta un proseso kompleho ku ta enbolbí akumulashon di proteina abnormal, inflamashon i disfunshon neuronal.
E dos karakterístikanan prinsipal di Alzheimer ta e presensia di plaka beta amiloide (Aβ) i tangle neurofibrillar (NFT) den e serebro.
Placa di beta-amiloide ta wordo forma ora fragmentonan di e proteina precursor di amiloide (APP) ta wordo kibra pa enzimanan pa forma peptido Aβ.
E peptidonan aki ta agregá i forma fibrilnan insolubel ku ta akumulá pafó di neuron, kibrando komunikashon di sèl pa sèl i kondusí na morto di neuron.
E akumulashon di Aβ plaka ta kere ta un di e promé eventonan den desaroyo di AD, i ta kere ta kontribuí na e proseso neurodegenerativo.
E tangle di neurofibril ta wordu forma ora e proteina tau wordu hiperfosforila i ta forma filamentonan anormal den neurona.
E 'tangles' aki ta stroba e funshonamentu normal di e mikrotubulonan, ku ta esensial pa transporte di nutriente i otro material den e neurona.
E konekshonnan ta hiba eventualmente na morto di e neuronnan afektá.
Inflamashon tambe ta hunga un ròl den e fisiopatologia di Alzheimer.
E sistema inmunológiko ta reakshoná riba akumulashon di Aβ plaka i NFT dor di liberá sitokina pro-inflamatorio, ku por oumentá e daño na neurona.
Ademas, tin evidensia ku strès oksidativo, disfunshon mitokondrial, i metabolismo di glukosa dañá ta kontribuí na e fisiopatologia di Alzheimer.
E faktornan aki por kondusí na disfunshon i morto di neurona, i asina e proseso di e malesa ta bira mas grave.
En general, e fisiopatologia di Alzheimer ta un interkambio kompleho di faktornan ku finalmente ta kondusí na e deterioro progresivo di funshon kognitivo i pèrdida di memoria ku ta karakterisá e malesa.
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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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