Kë ye cɔl 'Alzheimer's disease (AD)'ee tuany rac apɛi, man ye tuany cɔl 'Alzheimer's disease' bɛ̈n ya cɔ̈kpiny në mïïth tɔ̈c yiic, ku ka ye tuany cɔl 'inflammation' bɛ̈n ya cɔ̈kpiny në tuany de neuron yic.
Käŋ kaa rou ke AD aye tɔ̈u de amyloid-beta (Aβ) plaques ku neurofibrillary tangles (NFTs) në nhomic.
Amyloid-beta plaques aye kek looi të cenë biäk de amyloid precursor protein (APP) ya tek yiic në enzymes ago Aβ peptides ya cak.
Peptides aye röt määt ku loi kek kä cie lëu bïk röt ya liääp ku ye kek tääu në kä kɔ̈k peei yiic, ku ye cell-to-cell communication ya cɔk riääk ku ka neuronal thou.
Käk ye cɔl 'Aβ plaques' aye kek yök ëke ye tuany tueeŋ ye tuany de AD bɛ̈n cak, ku ka ye kek cɔk loi rot në puɔ̈ɔ̈c de neurodegenerative process yic.
Neurofibrillary tangles aye röt looi të cenë mïïth ke tau röt ya looi agokë ya tɔ̈ ëke ye mïïth ke neurons.
Kä cï röt thiääk käk aye luɔɔi de microtubules cɔk liääp, ye kä thiekiic cɔk loi röt në cäth de kä ye cam ku kä kɔ̈k peei tɔ̈ në neuron yic.
Kä cï röt thiääk aye kä cï röt thiääk ke neuron bɛ̈n ya nɔ̈k.
Tuanytuɛɛny aye röt looi në guɔ̈p de raan yic.
Ajuiɛɛr de gël de guɔ̈p ee rɔt dhuɔ̈k ago ciin de Aβ plaques ku NFTs ya juak në kë de cytokines ye tuanytuɛɛny bɛ̈ibei, man lëu bï kä ye tɔ̈ në puɔ̈ɔ̈n de raan ya juak apɛi.
Kë juɛ̈c, anɔŋ kä ye nyuɔɔth lɔnadɛ̈ ke oxidative stress, mitochondrial dysfunction, ku glucose metabolism cï riääk aye kä ye kɔc cɔk tuany në AD.
Kän alëu bï neuronal ya riɔ̈ɔ̈k ku bï thou, ku bï tuaany ya juak apɛi.
Në kë de abɛ̈n, ke puɔ̈ɔ̈c de tuaany de Alzheimer ee kë rilic apɛi ye rot looi në käjuëc yiic ku ka ye naŋ kë ye yen cɔk lɔ tueŋ ku ka ye nhom määr në ye tuany kënë yic.
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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