Ła patofisiologia del morbo de Alzheimer (MA) xe un proceso conpleso che coinvolge l'acumulo de proteine anomałi, infiamasion e disfunsion neuronałe.
I do segni principałi del MA xe a presensa de placche amiloide-beta (Aβ) e grovigli neurofibrillari (NFT) nel zervello.
Łe plache beta-amiloide łe se forma quando i frammenti deła proteina precursora amiloide (APP) i vien ciolti dai enzimi par formar peptidi Aβ.
Sti peptidi se unise e forma fibrille insolubiłi che se ingruma fora dei neuroni, disturbando a comunicasión tra cellule e portando ała morte dei neuroni.
L'accumulo de placche Aβ xe considerà uno dei primi eventi nel sviłupo del MA, e se crede che contribuisa al processo neurodegenerativo.
I grovigli neurofibrillari se forma quando a proteina tau diventa iperfosforilata e forma filamenti anormali dentro i neuroni.
Sti grovigli i interrompe el normale funsionamento dei microtubuli, che xe esensiài pal trasporto de nutrienti e altri materiali nel neurone.
I grovigli i porta ała morte dei neuroni colpìi.
L'infiamasion ga anca un ruolo neła patofisiologia del MA.
El sistema immunitario risponde a l'acumulo de placche Aβ e NFTs rilasciando citochine pro-infiammatorie, che pol agravar el dano ai neuroni.
Inoltre, ghe xe prove che el stress ossidativo, ła disfunsion mitocondriałe e el metabolismo del glucosio indebołìo contribuise ała patofisiologia del MA.
Sti fatori pol portar a disfunsion e morte neuronałe, aggravando ancora el proceso dea malatia.
In generale, a fisiopatologia del MA xe un'interasion conplesa de tanti fatori che in ultima analisi porta al declino progressivo neła funsion cognitiva e ała perdita de memoria che caraterixa a małatia.
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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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