Pathophysiology ya ugonjwa wa Alzheimer's ni nini?
Pathophysiology ya ugonjwa wa Alzheimer (AD) ni mchakato tata ambao unahusisha mkusanyiko wa protini zisizo za kawaida, uchochezi, na dysfunction ya neuronal.
Dalili mbili kuu za AD ni uwepo wa plaques za amyloid-beta (Aβ) na neurofibrillary tangles (NFTs) katika ubongo.
Vipande vya beta-amyloid hufanyizwa wakati vipande vya protini ya mtangulizi wa amyloid (APP) vinagawanywa na enzymes kuunda Aβ peptides.
Peptidi hizo hukusanyika na kufanyiza nyuzi zisizoweza kutoweka ambazo hukusanyika nje ya chembe za neva, zikivuruga mawasiliano kati ya chembe na chembe na kusababisha kifo cha chembe za neva.
Mkusanyiko wa Aβ plaques hufikiriwa kuwa moja ya matukio ya mapema katika maendeleo ya AD, na inaaminika kuchangia mchakato wa neurodegenerative.
Vipande vya neurofibrillary hufanyizwa wakati protini tau inakuwa hyperphosphorylated na huunda filaments zisizo za kawaida ndani ya neurons.
Vipande hivyo huvuruga utendaji wa kawaida wa mikrotubuli, ambazo ni muhimu kwa usafirishaji wa virutubisho na vifaa vingine ndani ya chembe ya neva.
Hatimaye mishipa hiyo husababisha kifo cha chembe za neva zilizoathiriwa.
Uchochezi pia una jukumu katika pathophysiology ya AD.
Mfumo wa kinga hujibu mkusanyiko wa Aβ plaques na NFTs kwa kutolewa pro-inflammatory cytokines, ambayo inaweza kuharibu uharibifu wa neurons.
Kwa kuongezea, kuna ushahidi kwamba mkazo wa oksidi, dysfunction ya mitochondrial, na kupungua kwa kimetaboliki ya sukari huchangia pathophysiology ya AD.
Sababu hizo zaweza kusababisha kasoro za utendaji wa neva na kifo, na kuharibu zaidi ugonjwa huo.
Kwa ujumla, pathophysiology ya AD ni mwingiliano tata wa mambo mengi ambayo hatimaye kusababisha kupungua kwa kasi katika kazi ya utambuzi na kupoteza kumbukumbu ambayo sifa ya ugonjwa.
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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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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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