Pathophysiology pole lasa Alzheimer (AD) iyanaritu proses kompleks iya muttama'e akumulasi protein abnormal, radang, nenniya disfungsi neuronal.
Duwa tanranna utama AD iyanaritu engkana amyloid-beta (Aβ) plaques nenniya neurofibrillary tangles (NFTs) ri ota'e.
Amiloid-beta plaques ribentu'i narekko fragmen protein pendahulu amiloid (APP) ripeccai pole enzim untu' mabbentu' peptida Aβ.
Peptida e ro aggregasi nenniya mabbentu fibril de'na wedding larut iya makkumulu ri saliweng neuron, nasolangi komunikasi sel-sel nenniya nassabari amatengna neuron.
Akkumulasi plak Aβ riasengngi mancaaji sala seddi kajajiang pammulang ri pallebangeng AD, nenniya riasengngi mabbantu lao ri proses neurodegeneratif.
Rilaleng iyae, tau protein mancaji hiperfosforilasi nenniya mabbentu filamen anormal rilaleng neuron.
Iyyae pakkakkasae nasolangi akkegunang normal mikrotubulus, iyya parellu untu' angkutan nutrisi nenniya bahan laingnge rilaleng neuron.
Padduppa'na napimping lao ri amatengna neuron iya nakennae.
Peradangan to maccule peran rilaleng patofisiologi AD.
Sistem kekebalan tubuh mappébali lao akkumulasi plak Aβ sibawa NFT sibawa leppessangngi sitokin pro-inflamasi, iya wedding napedeceng i ancurukeng lao ri neuron.
Rilalengna, engka butti makkeda stres oksidatif, disfungsi mitokondria, nenniya metabolisme glukosa iya de nacoco' makkacue ri patofisiologi AD.
Iyae faktor e wedding nassabari disfungsi neuronal nenniya amateng, lebbi napaenre proses lasa e.
Secara keseluruhan, patofisiologi AD iyanaritu interaksi kompleks pole maega faktor iya paccappureng nassabari ancurukeng progresif ri laleng fungsi kognitif nenniya ateddengeng memori iya mancaaji tanranna lasa e.
Nemeroff CB: The preeminent role of neuropeptide systems in the early pathophysiology of Alzheimer disease: up with corticotropin-releasing factor, down with acetylcholine. Arch Gen Psychiatry. 1999, 56 (11): 991-2.
Proft J, Weiss N: Jekyll and Hide: The two faces of amyloid β. Commun Integr Biol. 2012, 5 (5): 405-7.
Whitehouse PJ, Hedreen JC, White CL, Price DL: Basal forebrain neurons in the dementia of Parkinson disease. Ann Neurol. 1983, 13 (3): 243-8.
Casadesus G, Moreira PI, Nunomura A, Siedlak SL, Bligh-Glover W, Balraj E, Petot G, Smith MA, Perry G: Indices of metabolic dysfunction and oxidative stress. Neurochem Res. , 32 (4-5): 717-22.
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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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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