La fisiopatologjie de malatie di Alzheimer (MA) e je un procès complès che al cjape dentri la acumulazion di proteinis anormachis, la infiammazion e la disfunzion neuronâl.
I doi segns principâi dal DA a son la presince di plachis di beta-amiloide (Aβ) e gropis neurofibrilaris (NFTs) tal cerviel.
Lis plachis di beta-amiloide a si formin cuant che i framents de proteine precursore de amiloide (APP) a son taiâts dai enzimis par formâ peptidis Aβ.
Chescj peptidis a si agregin e a formin fibris insolubilis che si ingrumin fûr dai neurons, interuzion de comunicazion celule-celule e puartant ae muart dai neurons.
L'acumulament des plachis di Aβ al è considerât un dai prins events intal svilup de malatie di Alzheimer, e al è considerât un fatôr che al contribuìs al procès neurodegeneratîf.
I gropis neurofibrilaris a si formin cuant che la proteine tau e devente iperfosforilade e e forme filaments anormai dentri dai neurons.
Chescj gropaments a interuchin il funzionament dai microtubules, che a son essenziâi pal traspuart di nudriments e altris materiâi dentri dal neuron.
I gropaments a puartin ae muart dai neurons interessâts.
L'infiammazion e à ancje un rûl inte fisiopatologjie de malatie di Alzheimer.
Il sisteme imunitari al rispuint al cumulament des plachis Aβ e NFT molant fûr citochinis pro-infiammatoriis, che a puedin esacerbâ il dam ai neurons.
Cun di plui, a son evidencis che il stress ossidâtîf, la disfunzion mitocondriâl, e il metabolisim dal glucosi compromès a contribuissin ae patofisiologjie de AD.
Chescj fatôrs a puedin puartâ ae disfunzion neuronâl e ae muart, aggravant ancjemò di plui il procès de malatie.
In gjenerâl, la fisiopatologjie de malatie e je une interazion complesse di fatôrs che a puartin al declin progresîf des funzions cognitivis e ae pierdite de memorie che a caraterizin la malatie.
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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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