Patofiziologija Alzheimerove bolesti (AD) je složen proces koji uključuje akumulaciju abnormalnih proteina, upalu i neuronsku disfunkciju.
Dva glavna obilježja AD-a su prisustvo amiloid-beta (Aβ) plakova i neurofibrilarnih zamaka (NFT-ovi) u mozgu.
Amyloid- beta plake se formiraju kada se fragmenti amiloidnog prekursorskog proteina (APP) razdvajaju od strane enzima kako bi se formirali Aβ peptidi.
Ovi peptidi se agregiraju i formiraju nerastvorljive fibrile koje se akumuliraju izvan neurona, narušavajući komunikaciju između ćelija i dovodeći do smrti neurona.
Smatra se da je akumulacija Aβ plakova jedan od najranijih događaja u razvoju AD- a, i vjeruje se da doprinosi neurodegenerativnom procesu.
Neurofibrilarne zamke se formiraju kada protein tau postane hiperfosforiliran i formira abnormalne filamente unutar neurona.
Ove zamke ometaju normalno funkcionisanje mikrotubula, koji su od suštinskog značaja za transport hranljivih materija i drugih materijala unutar neurona.
Ove zamke na kraju dovode do smrti zahvaćenih neurona.
Upala takođe igra ulogu u patofiziologiji AD-a.
Imunološki sistem reaguje na akumulaciju Aβ plakova i NFT- a oslobađanjem proinflamatornih citokina, što može pogoršati oštećenje neurona.
Pored toga, postoje dokazi da oksidativni stres, mitohondrijska disfunkcija i oštećenje metabolizma glukoze doprinose patofiziologiji AD- a.
Ovi faktori mogu dovesti do disfunkcije neurona i smrti, dodatno pogoršavajući proces bolesti.
Sve u svemu, patofiziologija AD-a je složena interakcija više faktora koji na kraju dovode do progresivnog opadanja kognitivne funkcije i gubitka pamćenja koji karakterišu bolest.
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Candore G, Bulati M, Caruso C, Castiglia L, Colonna-Romano G, Di Bona D, Duro G, Lio D, Matranga D, Pellicanò M, Rizzo C, Scapagnini G, Vasto S: Inflammation, cytokines, immune response, apolipoprotein E, cholesterol, and oxidative stress in Alzheimer disease: therapeutic implications. Rejuvenation Res. , 13 (2-3): 301-13.
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Odricanje od odgovornosti: medicinski
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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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