Itī peptidi salosa kūpā i veidoj napuorītūšys fibrilis, kas uzkruoj uorpus neironu, traucūt šyunu komunikaceju i nūvadūt pi neironu smierts.
Teik skaiteits, ka Aβ plākšņu uzakruošona ir vīns nu agreimuokūs nūtykumu Alcheimera slimeibys atteisteibā i ka tys veicynoj neirodegenerativu procesu.
Neurofibrilarais saiteņu veidojās, kod proteins tau hiperfosforilējas i veidoj uorkuorteigus pavedīņus neironu īškīnē.
Itī saiteņi traucej mikrotubuleju parostajai funkcejai, kas ir svareigys uzturvīlu i cytu vīlu puorvītuošonai neirona īškā.
Piec laika pūsli nūvad pi ītekmātu neironu smierts.
Uorstiešona ari ir svareiga Alcheimera slimeibys patofiziologejā.
Imunys sistema reagej iz Aβ plākšņu i NFT uzakruošonu, atbreivojūt proinflamatorus citokinus, kas var padareit neironu būjuojumu vēļ stypruoku.
Pi tam ir pīruodejumi, ka oksidacejis stresa, mitohondreju disfunkceja i glikozis metabolisma trauciejumi ītekmej Alcheimera slimeibys patofiziologeju.
Itī faktori var izraiseit neironu disfunkceju i nuovi, vēļ vaira pasorgojūt slimeibu.
Kūpumā Alcheimera slimeibys patofiziologeja ir sarežgeita vairuoku faktoru sovstarpeiga īdarbeiba, kas gols golā nūvad pi progresivuos kognitivūs funkceju sasamazynuošonys i atmiņu zaudiešonys, kas ir slimeibys raksturs.
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.
['Atsaceišona nu: medicinys']
['Itei interneta vītne ir dūmuota tikai izgleiteibys i informacejis īmeslim, i tei nateik skaiteita par medicinys pīduovuojumu voi profesionalu pakolpuojumu.']
['Pīduovuotū informaceju nadreikst lītuot, kab diagnosticātu voi izuorstātu kaidu slimeibu, i tim, kas meklej personeigu mediciniskū padūmu, juosazynoj ar licencātu uorstu.']
['Juopīzeist, ka neironu teikls, kas generej atbiļdis iz vaicuojumim, ir eipaši napareizs, kod runoj par skaitliskū saturu, par pīmāru, par konkretu slimeibu diagnozātūs cylvāku skaitu.']
['Vysod meklejit padumu nu sova uorsta voi cyta kvalificāta uorsta, kab saprostu jiusu slimeibu. Nikod naatsakuortojit profesionalū uorsta padumu voi aizkavejit tū mekliešonu deļtuo, ka esat koč kū izlasiejs itamā interneta vītnē. Ka jiusim ruodīs, ka jiusim var byut uorsteibys uorkuortys situaceja, zvaniet 911 voi īīt tyvuokajā uorstnīceibys centrā.']
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['5. aplīcynuojumu, ka jiusu informaceja ir pareiza i ka jiusim ir tīseibys izmontuot autortīseibys, kuruos ir nūlīgts lītuot;']
['i 6) fizisks voi elektronisks autortīseibu turātuoja voi personas, kas ir pilnvarota dorbuotīs autortīseibu turātuoja vuordā, paraksts.']
['Lyudzu, syutiet mums e-postu ar sevkuru vaicuojumu/ieteikumu.']
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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