Oku kala kuove loku vela kuove ku pondola oku ku tuala koku vela kuenda oku ku tuala koku vela.
Ovituwa vivali via velapo vi lekisa uvei wo Alzheimer, oku kala kuovimatamata vimue viowoño vi tukuiwa hati, placas de beta-amiloide (Aβ) kuenda neurofibrillary tangles (NFTs).
Amiloide-beta plaques yi sokiyiwa eci olonepa vi proteína yitukuiwa okuti amiloide precursor (APP) vi tepiwa lovimatamata vi kuatisa oku panga o Aβ peptides.
Olopeptida viaco vi likongela kuenda vi linga oloneva ka vi yuliwa okuti vi liongoluila kosamua yoloneva, vi nyõla elitokeko liolo celula kuenda vi tuala kolofa violoneva.
Oku li vokiya kuovipuka vio Aβ ku tendiwa okuti ocina cimue catete ci lekisa oku fetika kuvei wo Alzheimer, kuenda ci tava okuti ci kuatisavo koku nyõleha kuolombuto.
Olombuanja vi tukuiwa hati, neurofibrillary vi sokiyiwa eci o proteína tau yi kuata o fosforilase yalua kuenda yi linga olonjita vimue ka via sungulukile vokati kolosinga.
Ovikolo viaco vi nyõla upange wovimatamata vi tukuiwa hati, microtubules, vi kuatisa koku ambata okulia kuenda ovina vikuavo viñila vo neurônio.
Noke, eci ci koka okuti, olo neurônios viaco vi fa.
Okufetika ku kuetevo onepa ko pathophysiology yo AD.
Uloño woku liteyuila kuvei u tambulula koku li vokiya kuovipuka vio Aβ kuenda NFT poku eca o citokines yi vetiya oku totomisa, okuti yi pondola oku vokiya evalo liolomakina.
Handi vali, kuli uvangi u lekisa okuti, esakalalo lioku kuata owule, ekambo liupange wovimatamata viuyali, kuenda ekambo lioku kuata uhayele wovimatamata viuyali, vi pondola oku nena uvei wo Alzheimer.
Ovina viaco vi pondola oku nyõla owoño womunu kuenda oku u tuala kolofa.
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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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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