Te peptydy agregowajōm sie i tworzōm nierozpuszczalne włōkiynka, kere grōmadzōm sie poza neurōnami, zaburzajōnc kōmunikacyjo miyndzy kōmōrkami i kludzōnc do śmierci neurōnōw.
Uwożo sie, iże akumulacyjo blaszek Aβ je jednym z nojwczasniyjszych zdarzyń we rozroście choroby Alzheimera i prziczynio sie do procesu neurodegeneracyjnego.
Neurofibrillarne plōntania tworzōm sie, kej biołtko tau ulega hiperfosforylacyji i tworzi niyôbyczajne włōkiynta we postrzodku neurōnōw.
Te plōntania zaburzajōm normalne funkcjōniyrowanie mikrotubuli, kere sōm zdatne do transportu skłodnikōw ôdżywczych i inkszych materyji we postrzodku neurōnu.
Te sploty na kōniec kludzōm do śmierci dotkniętych neurōnōw.
Zapalynie ôdegrowo tyż rola w patofizjologiji choroby Alzheimera.
Ukłod ôdpornościowy ryaguje na akumulacyjo blaszek Aβ i NFT bez uwolniynie prozapalnych cytokin, co mogōm pogorszyć zniszczynie neurōnōw.
Pōnadto sōm dowody na to, iże stres ôksydacyjny, dysfunkcyjo mitochōndriōw i zaburzōny metabolizm glukozy prziczyniajōm sie do patofizjologije choroby Alzheimera.
Te faktory mogōm kludzić do dysfunkcyje i śmierci neurōnōw, co jeszcze barzij zaostrzo proces chorobowy.
Ôgōlnie patofizjologijo choroby Alzheimera je słożōnym ôddziaływaniym mocy faktorōw, co na kōniec kludzōm do postympujōncego spodku funkcyje kognitywnych i utroty pamiyńci, co karakteryzuje ta choroba.
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.
Schindler SE, McConathy J, Ances BM, Diamond MI: Advances in diagnostic testing for Alzheimer disease. Mo Med. , 110 (5): 401-5.
Singh VK: Immune-activation model in Alzheimer disease. Mol Chem Neuropathol. , 28 (1-3): 105-11.
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['Zawiadōmiynia muszōm być posłane we formie pisymnyj bez email (adres email zob. sekcyjŏ "Kōntakt").']
['DMCA wymogo, coby Twoje zawiadōmiynie ô rzekōmyj naruszynie praw autorskich zawiyrało nastympujōnce informacyje: (1) ôpis roboty chroniōnyj prawami autorskimi, co je przedmiotym rzekōmyj naruszynio; (2) ôpis rzekōmyj naruszajōncyj zawartości i informacyje stykajōnce, coby przizwolić nōm na zlokalizowanie zawartości; (3) informacyje kōntaktowe ô Tobie, w tym Twōj adres, numer telefonu i adres e-mail; (4) ôświadczynie ôd Ciebie, iże wiysz we dobro wierze, iże zawartość we spōsobie, co ô nim sie skarżysz, niy ma autoryzowano ôd posiedziciela praw autorskich abo jego agynta, ani bez żodne prawo.']
['5) oświadczynie złożōne bez Ciebie, podpisane pod sztrŏfōm fałszywyj ôświadczyniŏ, iże informacyje zawarte we zawiadōmiyniu sōm akuratne i iże posiadasz uprawniynia do egzekwowaniŏ uprawniyń, co ône sōm rzekōmo naruszane;']
['i (6) fizyczny abo elektrōniczny podpis posiedziciela praw autorskich abo ôsoby upoważniōnyj do fungowanio w jego imiyniu. ']
['Niyôstawiynie wszyjskich powyższych informacyji może skutkować ôpōźniyniym we rozpatrzeniu skargi.']
['Kōnakt']
['Proszymy ô e-mail z kożdym pytaniym abo sugestijōm.']
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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