Bãaga bãaga (AD) yaa bũmb sẽn yaa toogo, tɩ poroteẽ rãmb sẽn pa sõma, põosgo, la neerã tʋʋm yood kẽed a pʋgẽ.
Bã-kãsems a yiib nins sẽn kɩtd tɩ ned tar AD yaa bãas sẽn yaa amyloïde-bêta (Aβ) sẽn be a zugã, la bãas a taab sẽn be a zugã.
Amiloid-beta plaques wã yaa bũmb sẽn maand tɩ amyloid precursor protein (APP) wã b sẽn boond tɩ proteins nins sẽn yaa pipi bõn- naandgã sã n wa kẽ n lebg Aβ peptide.
Yaa bõn-kãens n kɩtd tɩ ninsaal yĩngã wil fãa pa tõe n lagem taab n maan bũmb ye.
B tagsdame tɩ yaa bãagã sẽn wat ne bãas ninsã sʋka, yaa bã-kãng n sɩngd n kʋʋd nebã.
Neurofibrillary tangles wã yaa bũmb sẽn maand ne poroteẽ ning b sẽn boond tɩ tau wã sẽn lebg zũud tɩ loog noor n kɩt tɩ b lebg wa peen-vɩɩs sẽn pa sõma.
Bõn-kãens sẽn yaa toɛy-toɛyã sãamda mikro-tõodã sẽn tʋmd sõma wã, bala b yaa tɩlae ne-b tɩ b tall rɩɩb la bõn-yood a taab n kẽng neerã pʋgẽ.
Bãngdbã yeelame tɩ yaa b sẽn na n maan woto wã la b na n tõog n bãng bũmb ning sẽn kɩt tɩ ninsaal yam-yãkrã pa sõma wã.
Bãaga leb n tara a tʋʋmde.
Sull ning sẽn geta bãaga yell leokda bãaga sẽn wat ne plaques Aβ la NFTs sẽn kẽed ne bãaga wɛɛngẽ n yiisd cytokines sẽn wat ne bãaga, tɩ rẽ tõe n paas bãaga pãng ne neuronesã.
Sẽn paase, b wilgame tɩ bãagã sẽn wat ne bũmb ninsã yaa sũ-sãams sẽn yit yĩngã pʋgẽ, mitochondrial tʋʋm- wẽnga, la glikoz yĩngã wils sẽn pa tʋmd sõma wã.
Bõn-kãensã tõe n kɩtame tɩ bãagã paasdẽ, tɩ b pa le tʋmd sõma, tɩ b kiidẽ.
Sẽn yɩɩd fãa, bãagã sẽn wat ne yɛl ninsã fãa tara taaba.
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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.
['Bãngr-gomde: logtoeemdã']
['Yaa zãmsg la kibay kũun yĩng bal la b yiisd sit kãngã, la pa logtoeemdã wɛɛngẽ sagls bɩ tʋʋm-sõng maaneg yĩng ye.']
['B pa segd n tũnug ne kɩbay nins b sẽn kõ wã n bao bãag bɩ zu-loɛɛg tɩɩm ye. Sẽn dat-b tɩbsg b toor segd n tɩ yãa logtor sẽn tar sor n tõe n tɩp-ba.']
['D tẽeg tɩ b sẽn maand to-to n leokd sogsgã to-to wã pa zems ye.']
['Y sã n wa karemd bũmb sẽn be sɩtã pʋgẽ, bɩ y ra tol n yĩm tɩ y segd n tɩ gesa logtor ye. Y sã n tagsdẽ tɩ y tara yĩn-wɩsgr yell bɩ y bool 911 wall y kẽng logtor yirã.']
['Bas-m-yam: sɛbã zãab wɛɛngẽ']
['Digital Millennium Copyright Act sẽn yaa yʋʋmd 1998 soabã, 17 U.S.C. § 512 (DMCA) kõta sor tɩ ned sã n tẽed tɩ bũmb sẽn be ẽntɛrnetã pʋgẽ kɩɩsda a sẽn tar sor n tõe n maan bũmb ninsã, a tõe n tɩ kos n paam n lebse.']
['Yãmb sã n tẽed ne pʋ-peelem tɩ bũmb sẽn be tõnd sɩt wɛɛbã pʋgẽ bɩ tõnd tʋʋm-noyã pʋsẽ n sãamd yãmb dʋrwa wã, yãmb (bɩ y tʋʋm-tʋmdã) tõe n toola tõnd koɛɛg n kos tɩ d yiis bũmbã wall d gɩdg tɩ y ra paam n kẽ ye.']
['B segd n tʋma koees ne ẽtɛrnetã (Ges-y ẽtɛrnetã adɛrs sẽn be babg ning sẽn yet tɩ "Tõnd sõsg zĩigã").']
['DMCA wã baoodame tɩ yãmb sẽn na n togs ned tɩ b maan-a-la bũmb sẽn kɩɩsd a sẽn tar sor n tõe n maan bũmb ningã, bɩ y wilg-a bũmb nins sẽn pʋgdã: 1) bũmb ning sẽn kɩt tɩ b maan-a bũmb ningã, 2) bũmb ning sẽn kɩt tɩ b maan-a bũmb ningã, la y wilg-d bũmb ning sẽn kɩt tɩ d tõe n bãng a sẽn be zĩig ninga. 3) y sẽn tõe n paam ned n gom ne-a to-to, n paas y adɛrsã, telefõnnã nimero, la y e-mailã. 4) y sã n yeel tɩ y kɩsa sɩd tɩ bũmb ning sẽn kɩt tɩ y maan bũmb ningã pa ned ning sẽn tar sor n tõe n maan bũmbã, bɩ a tʋm-tʋmdã, bɩ laloa wã sẽn kõ sor tɩ y maan ye.']
['5) Y sã n wa rat n wilg tɩ y pa tar sor n na n kɩɩs ned a to, bɩ y gʋls sebr n wilg tɩ y sẽn togsã yaa sɩda, la tɩ y tara sor n na n wilg tɩ nedã sẽn maan bũmb ning n kɩɩs yãmb dʋrwa rãmbã yaa sɩda.']
['La (6) sɛb nins sẽn tar-b sor n na n yiis sɛbã, bɩ ned sẽn tar sor n na n tʋm sɛbã yiisg yĩngã.']
['Y sã n pa gʋls kibay nins sẽn be yĩngrã, tõe n kɩtame tɩ y yẽgengã kaoos n pa sa ye.']
['Sõsg ne neda']
['Y sã n tar sokr bɩ y sẽn dat n bãnge, bɩ y gʋls-d lɛtr n tool-do.']
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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