Àìsàn Alzheimer (AD) jẹ́ ètò tí ó díjú tí ó ní í ṣe pẹ̀lú àkójọpọ̀ àwọn èròjà protein tí kò bára dé, ìdààmú, àti àìsàn àwọn ẹ̀yà ara.
Àwọn àmì pàtàkì méjì tí àrùn Alzheimer ní ni pé ó ní àwọn èròjà amyloid-beta (Aβ) nínú ọpọlọ àti àwọn èròjà neurofibrillary tangles (NFTs) nínú ọpọlọ.
Àwọn àlàfo amyloid- beta máa ń dá sílẹ̀ nígbà tí àwọn èròjà amyloid precursor protein (APP) bá di èyí tí àwọn èròjà amyloid máa ń ya sọ́tọ̀ láti ṣe àwọn Aβ peptides.
Àwọn peptides wọ̀nyí máa ń kóra jọ, wọ́n sì máa ń di àwọn fibril tí kò ṣeé tú sínú ara tí wọ́n sì máa ń kóra jọ níta inú ẹ̀yà ara, èyí sì máa ń ba àjọṣe tó wà láàárín sẹ́ẹ̀lì àti sẹ́ẹ̀lì jẹ́, èyí sì máa ń yọrí sí ikú ẹ̀yà ara.
A gbagbọ pe ikojọpọ ti awọn pẹpẹ Aβ jẹ ọkan ninu awọn iṣẹlẹ akọkọ ni idagbasoke ti AD, ati pe a gbagbọ pe o ṣe alabapin si ilana neurodegenerative.
Àwọn àlàfo neurofibrillary máa ń wáyé nígbà tí èròjà protein tau bá di hyperphosphorylated, ó sì máa ń di àwọn àlàfo tí kò bófin mu nínú àwọn ẹ̀yà ara.
Àwọn kòkòrò yìí máa ń ba iṣẹ́ tí wọ́n ń pè ní microtubules jẹ́ jẹ́, wọ́n sì ṣe pàtàkì gan-an fún bí wọ́n ṣe ń gbé àwọn èròjà tó ń fúnni lókun àti àwọn nǹkan mìíràn sínú ẹ̀yà ara.
Ní àsẹ̀yìnwá àsẹ̀yìnbọ̀, àwọn sẹ́ẹ̀lì ọpọlọ tó ní àrùn náà máa ń kú.
Ìjàgà tún ń kó ipa pàtàkì nínú bí àrùn Alzheimer ṣe ń wáyé.
Ilana ajẹsara dahun si ikojọpọ ti Aβ plaques ati NFTs nipa itusilẹ awọn cytokines pro-inflammatory, eyiti o le mu ibajẹ si awọn neurons pọ si.
Pẹlupẹlu, ẹri wa pe wahala oxidative, dysfunction mitochondrial, ati aiṣedede iṣelọpọ glucose ṣe alabapin si pathophysiology ti AD.
Àwọn nǹkan wọ̀nyí lè mú kí àwọn ẹ̀yà ẹ̀yà ara má ṣiṣẹ́ dáadáa, kí wọ́n sì kú, èyí sì lè mú kí àìsàn náà le sí i.
Ni gbogbogbo, pathophysiology ti AD jẹ ibaraenisepo idiju ti ọpọlọpọ awọn ifosiwewe ti o pari si idinku ilọsiwaju ni iṣẹ oye ati pipadanu iranti ti o ṣe afihan arun naa.
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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Ìfọ̀rọ̀wérọ̀
Jọwọ fi imeeli ranṣẹ si wa pẹlu eyikeyi ibeere / imọran.
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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