Alzheimer's disease (AD) natna hi thil khirh tak a ni a, chutah chuan protein ṭha lo a pung a, a lo vâwt a, neuron hna a thawk ṭha lo ṭhîn.
AD natna chhinchhiahna pawimawh tak pahnih chu thluaka amyloid-beta (Aβ) plaques leh neurofibrillary tangles (NFTs) awm hi a ni.
Amyloid-beta plaque chu amyloid precursor protein (APP) chu enzyme hmangin Aβ peptides siam nân a inṭhen darh hian a lo awm a.
Chûng peptides-te chu an inpawlh a, neuron pâwn lama pungkhâwm, cell-to-cell inbiakpawhna tibuaiin, neuron thihna thlen thei fibril te an siam a ni.
Aβ plaque pung chhoh chu AD natna lo chhuahna bulpui ber nia ngaih a ni a, chu chuan neurodegenerative process a thlen niin an ring.
Neurofibrillary tangles hi protein tau chu hyperphosphorylated a nih a, neuron chhûngah chuan filaments mumal lo tak a siam hian a lo awm a ni.
Chûng thilte chuan microtubule-te hna pangngai chu a tibuai a, chu chu neuron chhûnga chaw leh thil dang phurh luh nâna pawimawh tak a ni.
A tâwpah chuan, chu inpawlhna chuan a nghawng neuron-te chu a tihlum ta a ni.
Pumpui natna hian Alzheimer natna awm dân pawh a hril bawk.
Immune system chuan Aβ plaques leh NFTs pungkhawm chu pro-inflammatory cytokines tichhuakin a chhang a, chu chuan neuron te a tichhe zual thei a ni.
Chu bâkah, oxidative stress, mitochondrial dysfunction, leh glucose metabolism chhe lutukte chuan Alzheimer natna a thlen tih finfiahna a awm bawk.
Chûng thilte chuan neuron hna a thawh ṭhat loh phah thei a, a thihtîr thei a, chu chuan natna chu a tizual thei a ni.
A tlângpui thuin, Alzheimer natna chu thil tam tak inzawmkhâwmna khirh tak a ni a, chu chuan a tâwpah chuan natna târ langtu hriatna hna thawhna ṭhat lohzia leh hriatna bozia a thlen a ni.
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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