Patofiziologija Alzheimerjeve bolezni (AD) je zapleten proces, ki vključuje kopičenje nenormalnih beljakovin, vnetje in nevronske disfunkcije.
Dve glavni značilnosti Alzheimerjeve bolezni sta prisotnost amiloid-beta (Aβ) plošč in nevrofibrilarnih zapletov (NFT) v možganih.
Amyloid- beta plošče nastanejo, ko so fragmenti amiloidnega predhodnega beljakovine (APP) razcepljeni z encimi in tvorijo Aβ peptide.
Ti peptidi se združijo in tvorijo netopljive fibrile, ki se kopičijo zunaj nevronov, kar moti komunikacijo med celicami in vodi do smrti nevronov.
Domneva se, da je kopičenje Aβ plakov eden najzgodnejših dogodkov pri razvoju AD in da prispeva k nevrodegenerativnemu procesu.
Neurofibrilarni zaplet se tvori, ko protein tau postane hiperfosforiliran in tvori nenormalne filamente znotraj nevronov.
Te zapletenosti motijo normalno delovanje mikrotubul, ki so bistvenega pomena za prevoz hranil in drugih materialov znotraj nevrona.
Te zapletenosti sčasoma privedejo do smrti prizadetih nevronov.
Vnetje igra tudi vlogo v patofiziologiji Alzheimerjeve bolezni.
Imunski sistem se odzove na kopičenje Aβ plakov in NFT-jev z sproščanjem pro- vnetnih citokinov, ki lahko poslabšajo poškodbe nevronov.
Poleg tega obstajajo dokazi, da oksidativni stres, mitohondrijska disfunkcija in motena presnova glukoze prispevajo k patofiziologiji Alzheimerjeve bolezni.
Ti dejavniki lahko privedejo do nevronske disfunkcije in smrti, kar še dodatno poslabša proces bolezni.
Na splošno je patofiziologija Alzheimerjeve bolezni zapleten medsebojni vpliv več dejavnikov, ki na koncu vodijo do postopnega upada kognitivnih funkcij in izgube spomina, ki je značilna za bolezen.
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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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Opozorilo: medicinsko
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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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