Alzheimer gaixotasunaren patofisiologia (AD) prozesu konplexua da, proteina anormalen metaketa, hantura eta neuronen disfuntzioa barne hartzen dituena.
ADren bi ezaugarri nagusiak amiloide-beta (Aβ) plakak eta neurofibrilarren (NFT) nahasketa garunean egotea dira.
Amiloide-beta plakak sortzen dira amiloide-aurreko proteinaren (APP) zatiak entzimek zatitzen dituztenean Aβ peptidoak osatzeko.
Peptido horiek biltzen dira eta neuronen kanpoaldean metatzen diren fibrila disolbaezinak osatzen dituzte, zelula-zelula komunikazioa etenez eta neuronen heriotzara eramanez.
Aβ plaken metaketa ADren garapenerako lehen gertaeretako bat dela uste da, eta neurodegeneratzaile prozesuari laguntzen diola uste da.
Neurofibrilarren korapiloak sortzen dira tau proteina hiperfosforilatzen denean eta neuronen barruan filamentu anormalak osatzen dituenean.
Sare horiek mikrotubuluen funtzionamendu normala oztopatzen dute, funtsezkoak baitira elikagaiak eta beste material batzuk garraiatzeko neuronen barruan.
Azkenean, neurona kaltetuak hiltzen dira.
Hanturak ere paper bat jokatzen du ADren patofisiologian.
Immunitate-sistemak Aβ plaken eta NFTen metaketari erantzuten dio zitokina proinflamatorioak askatzen dituela, neuronen kalteak areagotu ditzaketenak.
Gainera, badira ebidentziak estres oxidatiboak, mitokondrioen disfuntzioak eta glukosaren metabolismoaren narriadurak ADren patofisiologiari laguntzen diotela.
Faktore horiek neuronen disfuntzioa eta heriotza eragin ditzakete, gaixotasunaren prozesua areagotuz.
Orokorrean, ADren patofisiologia faktore anitzen elkarrekintza konplexua da, azkenean gaixotasunari ezaugarritzen dion funtzio kognitiboaren beherakada progresiboa eta memoria galera dakartzana.
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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