Pathophysiologydo kwasa Alzheimerbe (AD) dǝ shima diwal donyi tajirwa donyi kǝltǝwu protin be jili gade ma, kǝntǝwutǝ, a zǝktǝram neuron be.
Alamwa indi kambowo donyi AD be sandima plaques a amyloid-beta (Aβ) a neurofibrillary tangles (NFT) kǝrǝn lan.
Amyloid-beta plaques sawu duwal gənatəyin shi protein do sha sutuluyin ma (APP) də wa enzymes ya yi na lan gənatin.
Peptides sandima anyi na fallo kəltayin, fibrils donyi sulumaro katiyi bawo, sandidonyi fuwu zarra so dən gənatin, adəye cell-to-cell communication dəa kalzəyin, kuru neuronal death ro suwudin.
Samno daso Aβ plaquesbedə shima baditəram awoa fuwulan wakajin AD bero təma, kuru banazəgə kəndaram neurodegenerativebe suwudin.
Neurofibrillary tangles də sa protein tau ye hyperphosphorylated ro waljiya aw filaments la tiyi neuron yen gənatin.
Tartip donyi kǝltǝma dǝ, cida donyi microtubules be dabsǝna, shidonyi faidawa kǝnzambi be su zama, awu gabil ma a nasha la awu suro neuron be lan.
Kәnzәli dәye kuru kәndowa suro pathophysiology AD ye dәn mbeji.
Fasal nzǝliwo be du bayan sawandin kǝla tartip donyi Aβ plaques a NFTs a lan, citokines donyi kǝla kwasa be lan kara, shi donyi neuron ro banna suwudin ma.
Samma son, shi pathophysiology ADbedə zaumaro kaziyiya kada suronzən mbeji kuru adəbe səkə daji lamarra hangal gənatəgə asutəa kuru taktəa futu shi kasuwa adə dagəna dəga taidazə bannajin.
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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