Ny pathophysiology ny aretin'i Alzheimer (AD) dia dingana sarotra izay ahitana ny fanangonan-karena ny tsy ara-dalàna ny proteinina, mamaivay, ary neuronal dysfunction.
Ny fisehoan'ny takelaka beta-amyloïde (Aβ) sy ny tangles neurofibrillary (NFT) ao amin'ny atidoha no tena mampiavaka ny aretin'i Alzheimer.
Ny plaque amyloïde-beta dia miforona rehefa vaky ny ampahany amin'ny proteinina amyloïde precursor (APP) amin'ny alàlan'ny anzima mba hamorona peptides Aβ.
Ny fivangongoan'ny takelaka Aβ dia heverina ho iray amin'ireo tranga voalohany indrindra amin'ny fivoaran'ny AD, ary inoana fa mandray anjara amin'ny fizotran'ny neurodegenerative.
Miforona ny tangles neurofibrillary rehefa lasa hyperphosphorylated ny proteinina tau ary mamorona filament tsy mahazatra ao anatin'ny neurons.
Manelingelina ny fiasan'ny mikrotubula ireo zavatra mifatotra ireo, izay tena ilaina amin'ny fitaterana ireo otrikaina sy zavatra hafa ao anatin'ny neuron.
Lasa maty ireo sela voan'ilay aretina, rehefa ela ny ela.
Ny hery fiarovana dia mamaly ny fivontosan'ny takelaka Aβ sy ny NFT amin'ny alàlan'ny famoahana cytokines pro-inflammatory, izay mety hampitombo ny fahasimban'ny neurons.
Ankoatra izany, misy porofo fa ny adin-tsaina amin'ny oxidative, ny tsy fetezan'ny mitochondrial, ary ny tsy fahampian'ny metabolisma glucose dia mandray anjara amin'ny pathophysiology an'ny AD.
Mety hanimba ny fiasan'ny rafi-pitatitra sy hahafaty azy ireny, ka vao mainka hiharatsy ny aretina.
Amin'ny ankapobeny, ny fizika ara-pahasalaman'ny aretin'i Alzheimer dia fifandraisan'ny anton-javatra maro izay mitarika amin'ny fihenan'ny fiasan'ny saina sy ny fahaverezan'ny fitadidiana izay mampiavaka ny aretina.
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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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['Fifandraisana']
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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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