O le ā le pathophysiology o le maʻi o le Alzheimer?
O le pathophysiology o le faamaʻi o le Alzheimer (AD) o se faagasologa lavelave e aofia ai le faaputuputuina o polotini e lē masani ai, le fulafula, ma le lē lelei o galuega a neula.
O vala autū e lua e iloa ai le AD, o le iai o ni vaega o le sela e taʻu o le amyloid-beta (Aβ) ma ni vaega o le sela e taʻu o le neurofibrillary tangles (NFT) i le faiʻai.
E maua mai le amyloid-beta plaques pe a vaevaeina e le enzyme ni vaega o le amyloid precursor protein (APP) e maua mai ai le Aβ peptides.
O nei peptides e faaputuputu ma faia ai ni fibrils e lē mafai ona liusuavai, ma faaputuputu i fafo o sela o le neula, ma faaleagaina ai fesootaʻiga i le va o sela ma iʻu ai ina feoti sela o le neula.
O le faaputuputuina o Aβ plaques ua manatu o se tasi o mea muamua na tutupu i le atinaʻeina o le AD, ma e talitonu e fesoasoani i le neurodegenerative process.
E maua mai le neurofibrillary tangles pe a soona faamamāina le protein tau ma maua ai ni filament e lē masani ai i totonu o neula.
O nei mea e lē mafai ona gaoioi lelei ai ia vaega ninii o le sela, lea e tāua mo le feaveaʻi o meaʻai ma isi mea i totonu o le sela.
O nei mea e fesootaʻi faatasi, e iʻu ina mamate ai sela o le faiʻai ua aafia.
E iai foʻi se vaega a le mumū i le pathophysiology o le AD.
O le faiga puipuia e tali atu i le faaputuputuina o Aβ plaques ma NFTs e ala i le faamatuu mai o le pro-inflammatory cytokines, lea e mafai ona faateteleina ai le faaleagaina o neula.
E lē gata i lea, e iai faamaoniga e faapea o le mafatia i le okesene, lē lelei o galuega a mitochondrial, ma le lē lelei o le glucose metabolism, e aafia ai le pathophysiology o le AD.
O nei vala e mafai ona māfua ai le lē lelei o galuega a neula ma oo ai ina feoti, ma atili ai ona faateteleina le maʻi.
I se tulaga lautele, o le pathophysiology o le AD o se faiga lavelave o vala eseese ia e iʻu ai i le faasolosolo mālie ona faaitiitia o le mafaufau ma le lē manatuaina o mea e masani ai le faamaʻi.
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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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