Pathophysiology ya bolwetši bja Alzheimer (AD) ke tshepedišo e raraganego yeo e akaretšago go kgobokana ga diproteine tše di sa tlwaelegago, go ruruga le go se šome gabotse ga di-neuron.
Dika tše pedi tše dikgolo tša bolwetši bja Alzheimer ke go ba gona ga di-plaque tša amyloid-beta (Aβ) le di-neurofibrillary tangles (NFTs) ka bjokong.
Di-plaque tša amyloid-beta di bopega ge dikarolwana tša proteine ya pele ga amyloid (APP) di kgaolwa ke di-enzyme go bopa di-peptide tša Aβ.
Di-peptide tše di a kgobokana gomme tša bopa di-fibril tše di sa tologego tšeo di kgobokanago ka ntle ga di-neuron, tša šitiša poledišano ya sele le sele gomme tša lebiša lehung la di-neuron.
Go naganwa gore go kgobokana ga di-plaque tša Aβ ke se sengwe sa ditiragalo tša pele-pele tša go tšwelela ga AD, gomme go dumelwa gore go tlaleletša go tshepedišo ya go senyega ga bjoko.
Di-tangle tša di-neurofibrillary di bopša ge proteine tau e ba le hyperphosphorylated gomme e bopa ditlhale tše di sa tlwaelegago ka gare ga di-neuron.
Di-tangle tše di šitiša go šoma ka tsela e tlwaelegilego ga di-microtubule, tšeo di lego bohlokwa bakeng sa go rwala phepo le dilo tše dingwe ka gare ga neuron.
Mafelelong go raragana mo go feleletša ka go hwa ga di-neuron tšeo di kgomilwego.
Go ruruga gape go kgatha tema go pathophysiology ya AD.
Tshepedišo ya go lwantšha malwetši e arabela go kgoboketšo ya di-plaque tša Aβ le di-NFT ka go lokolla di-cytokine tša go hlohleletša go ruruga, tšeo di ka gakatšago tshenyo ya di-neuron.
Go oketša moo, go na le bohlatse bja gore kgateletšego ya go šilafala, go se šome gabotse ga mitochondrial le go senyega ga go šilega ga glucose di tlaleletša go pathophysiology ya AD.
Dilo tše di ka lebiša go se šome gabotse ga ditšhika tša bjoko le go hwa ga tšona, tša gakatša bolwetši le go feta.
Ka kakaretšo, pathophysiology ya AD ke go kgokagana mo go raraganego ga dilo tše dintši tšeo mafelelong di lebišago go senyegeng ga tšwelopele ya go šoma ga monagano le go lahlegelwa ke monagano mo go hlaolago bolwetši.
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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.
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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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