La fisiopatologia de la malautiá d'Alzheimer (MA) es un procediment complèxe que consistís en l'acumulacion de proteïnas anormalas, inflamacion, e disfoncion neuronala.
Las doas caracteristicas principalas de la malautiá son la preséncia de placas de beta amiloïda (Aβ) e de gropaments neurofibrillars (NFT) dins lo cervèl.
Las placas beta amiloïdas se forman quand de fragments de la proteïna precursora amiloïda (APP) son trencadas per d'enzims per formar de peptids Aβ.
Aqueles peptids s'agregan e forman de fibrillas insolublas que s'acumulant fòra dels neurònas, trencan la comunicacion cellula-a-cellula e menant a la mòrt neuronala.
L'acumulacion de las placas Aβ se pensa èsser un dels primièrs eveniments dins lo desvelopament de la malautiá d'Alzheimer, e se crei que contribuís al procediment neurodegeneratiu.
Los embolhs neurofibrillars se forman quand la proteïna tau ven iperfosforilada e forma de filaments anormals a l'interior dels neuròns.
Aqueles embolhs perturban lo foncionament normal dels microtubuls, que son essencials pel transpòrt dels nutriments e autres materials dins lo neuròn.
Los embolhs acaban per provocar la mòrt dels neuròns tocats.
L'inflamacion tanben ten un ròtle dins la fisiopatologia de la malautiá d'Alzheimer.
Lo sistèma immunitari respond a l'acumulacion de las placas Aβ e NFTs liberant de citoquinas proinflamatòrias, que pòdon agravar lo damatge als neurònas.
Mai, i a d'evidéncias que l'estrès oxidatiu, disfoncion mitocondriala, e lo metabolisme del glucòsa mermat contribuisson a la fisiopatologia de la malautiá d'Alzheimer.
Aqueles factors pòdon menar a un disfoncionament neuronal e a la mòrt, agravant encara lo procediment de la malautiá.
La fisiopatologia de la malautiá d'Alzheimer es una interaccion complèxa de factors multiples que menan fin finala a la baissa progressiva de la foncion cognitiva e a la pèrda de memòria que caracteriza la malautiá.
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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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