Cudurka Alzheimers (AD) waa geedi socod adag oo ku lug leh uruurinta borotiinka aan caadiga ahayn, caabuqa, iyo cilladaha neerfaha.
Labada astaamood ee ugu muhiimsan ee AD waa jiritaanka amyloid-beta (Aβ) plaques iyo neurofibrillary tangles (NFTs) ee maskaxda.
Amyloid-beta plaques waxaa la sameeyaa marka qaybo ka mid ah amyloid precursor protein (APP) ay kala jabaan enzymes si ay u sameeyaan Aβ peptides.
Peptides-yadani waxay isu ururiyaan waxayna sameeyaan xargaha aan la dareemi karin ee ku urursan neurons-ka dibadiisa, iyagoo carqaladeynaya isgaarsiinta unugyada unugyada waxayna keenaan dhimashada neuronal-ka.
Isku soo uruurinta Aβ plaques waxaa loo maleynayaa inay tahay mid ka mid ah dhacdooyinka ugu horreeya ee horumarinta AD, waxaana la rumeysan yahay inay gacan ka geysato geedi socodka neurodegenerative.
Xidhiidhka Neurofibrillary waxaa la sameeyaa marka borotiinka tau uu noqdo hyperphosphorylated oo uu sameeyo fiilooyin aan caadi ahayn gudaha neurons.
Xidhiidhadaasi waxay carqaladeeyaan shaqada caadiga ah ee microtubules-ka, kuwaas oo muhiim u ah gaadiidka nafaqooyinka iyo walxaha kale ee ku jira neuron-ka.
Xidhiidhku wuxuu ugu dambeyntii keenaa dhimashada unugyada neerfaha ee ay dhibaatadu saameysey.
Caabuqa ayaa sidoo kale door muhiim ah ka ciyaara pathophysiology ee AD.
Nidaamka difaaca jidhku wuxuu ka jawaabaa uruurinta Aβ plaques iyo NFTs isagoo sii deynaya cytokines-ka caabuqa, taas oo sii xoojin karta dhaawaca neerfaha.
Intaas waxaa sii dheer, waxaa jira cadeymo muujinaya in cadaadiska oksaydhka, cillad mitochondrial, iyo metabolism glucose oo xumaaday ay gacan ka geystaan pathophysiology-ka AD.
Guud ahaan, pathophysiology ee AD waa isdhexgalka adag ee arrimo badan oo ugu dambeyntii keena hoos u dhaca sii kordhaya ee shaqada garashada iyo luminta xusuusta ee astaamaha cudurka.
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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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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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