Altsgeýmer keseliniň patofiziologiyasy (AD) anormal proteinleriň birikdirilmegini, ýagyşlanmagy we neýronlaryň işlemeýişini öz içine alýan murekkep bir prosesdir.
AD-niň iki esasy nyşany beýnide amiloid-beta (Aβ) plaklary we neyrofibrillary tangles (NFTs) barlygy.
Amiloid-beta plaklary amiloid öňbaşly protein (APP) bölekleri Aβ peptidlerini döretmek üçin fermentler tarapyndan bölünende döredilýär.
Bu peptidler birikdiriler we neuronlaryň daşynda üýşýän çözünmeýän fibrillary döredýärler, bu bolsa hüceyreden hüceyre habarlaşmagy bozýar we neuron ölüminde sebäp bolýar.
Aβ plaklarynyň birikmegi AD-niň öňki ýagdaýlarynyň biri bolup, ol neýrodegenerativ prosesine goşant goşýar.
Neýrofibrillary torlamalar tau proteýni giperfosforyllaşyp, neýronlaryň içinde anormal syrylary döredende döredilýär.
Bu topaklar näzyron içindäki iýmitleri we başga materiallary äkitmek üçin esasy bolan mikrotübülleriň adaty işleýşini bozýar.
Bu çylşyrymlar soňunda täsir edilen neýronlaryň ölmegine eltýär.
Ýagşylyk hem AD-niň patofiziologiyasynda rol oýnaýar.
Immun sistemasy Aβ plaklary we NFT-leriň birikdirilmegine neyronlara zyýan ýetirmegi has beterleşdirýän pro-ýanyşykly sitokinleri boşatmak bilen jogap berýär.
Galyberse-de, oksidleşdiriji stres, mitokondriýa disfunksiýasy we şeker metabolizmasynyň bozulmagynyň AD-niň patofiziologýasyna goşant goşýandygy barada subutnamalar bar.
Bu zatlar kesel prosesini has beterleşdirýän neyronlaryň işlemeýändigine we ölmegine eltýär.
Umuman alanyňda, AD-niň patofiziologiyasy köp faktorlaryň kompleks birleşdirilmesidir welin, bu keselligiň aýratynlygy bolan biliş funksiýasynyň we ýatlama ukybynyň kemelýän ýitirimine eltýär.
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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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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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