Sa fisiopatologia de sa maladia de Alzheimer (MA) est unu protzessu cumplessu chi ìmplicat s'ammuntonamentu de proteinas anormales, infiammamentu e disfunzione neuronale.
Sos duos printzipales sinnos de sa maladia de Alzheimer sunt sa presèntzia de placas de amiloide-beta (Aβ) e sos grovos neurofibrillares (NFT) in su cherbeddu.
Sas placas de amiloide-beta si formant cando sos frammentos de sa proteina precursora de s'amiloide (APP) sunt segados dae sos enzimas pro formare sos peptides Aβ.
Custos peptides s'aggregant e formant fibrillas insolùbiles chi s'ammuntonant in foras de sos neurones, interrùmpende sa comunicatzione tra tzèllulas e giughende a sa morte neuronale.
S'ammuntonamentu de placas de Aβ si pensat chi siat unu de sos primos eventos in s'isvilupu de sa maladia de Alzheimer, e si pensat chi contribuat a su protzessu neurodegenerativu.
Sos grovos neurofibrillares si formant cando sa proteina tau si faghet iperfosforilada e format filamentos anormales a intro de sos neurones.
Custos grovos interrumpent su funtzionamentu normale de sos microtùbulos, chi sunt essentziales pro su trasportu de nutrientes e àteros materiales a intro de su neurone.
Sos ligàmenes a sa fine batint a sa morte de sos neurones interessados.
S'inflamatzione giogat fintzas unu ruolu in sa fisiopatologia de sa maladia de Alzheimer.
Su sistema immunitàriu rispondet a s'ammuntonamentu de placas Aβ e NFTs cun sa liberatzione de citocinas pro-inflamatòrias, chi podent aumentare sos dannos a sos neurones.
In prus, b'at proas chi s'istress ossidativu, sa disfuntzione mitocondriale e su metabolismu de su glucosiu diminuidu contribuint a sa fisiopatologia de sa MA.
Custos fatores podent batire a una disfunzione e morte neuronale, agravende in manera annanghedora su protzessu de sa maladia.
In generale, sa fisiopatologia de sa maladia de Alzheimer est un'interatzione cumplessa de fatores mùltiplos chi a sa fine batint a su declinu progressivu de sa funtzione cognitiva e a sa pèrdida de memòria chi caraterizat sa maladia.
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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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