Tasnudert n waṭṭan n Alzheimer (AD) d tamhelt yemgaraden i d-yettawin asebleɛ n teprutinin ur nṣeḥḥa ara, afulki, d tuffɣa n tezmert n yiẓuran.
Sin n yismawen imenza n waṭṭan n Alzheimer d tilin n yiɣbula n beta-amyloid (Aβ) d yiɣbula n neurofibrillary (NFTs) deg wallaɣ.
Tifekkiwin n beta-amyloid ttmaggant mi ara ttwagezmen yiḥricen n protein amyloid precursor (APP) s yienzimen akken ad d-snulfun ipuptiden Aβ.
Peptides-a ttemsegrawen u ttarran-d ifibrilen ur nferru ara i d-yettnejmaɛen deg berra n iẓuran, s wakka ttwaɣayen taywelt gar n tsilunin u ttawint ɣer tmettant n iẓuran.
Asemɣer n yiɣbula n Aβ yettwaḥsab d yiwen seg ineḍruyen imezwura deg unerni n waṭṭan n Alzheimer, yerna yettwaḥsab d win yettekkan deg usenfar n usnefli n yiẓuran.
Iẓewran n neurofibrillary ttmagen mi ara tuɣal tpurutint tau d tin yettwasemɣaren s waṭas yerna tga isuraf ur nṣeḥḥa deg yiẓewran.
Iẓewran-a ttwaɣen axeddim amatu n mikrutubulen, i ilaqen i usiweḍ n yiẓeḍwa d wallalen-nniḍen sdaxel n uẓar.
Iɣewwaren-a ttawin ɣer tagara ɣer tmettant n yiḥerqan yettuḍnen.
Asnefli yetturar daɣen tamlilt deg tfizitulujit n waṭṭan n Alzheimer.
Anagraw anaffal yettarra-d ɣef ujmaɛ n tfelwiyin n Aβ d NFTs s usuffeɣ n cytokines yettmuddun afares, izemren ad yessewεer lexṣara n yiẓuran.
Rnu ɣer waya, llant ttbutat i d-yeqqaren belli asnuffes n tnefsit, axeddim ur nṣeḥḥa n umitokondri, d usemdu n glucose ur nṣeḥḥa, d ayen i d-yettmuddun afus i tfesna n waṭṭan n Alzheimer.
Imgan-a zemren ad d-awin ɣer yir axeddim n yiḥellufen n yiɣes d tmettant, yerna ad rnun ad ssuɣulen aḍḍan n waṭṭan.
S umata, tafizitut n waṭṭan n Alzheimer d tamlilt yemgaraden n waṭas n yimgan yettawin ɣer tagara ɣer tneggarut n tmusni d tukksa n tektawt i d-yettbanen deg waṭṭan-a.
Nemeroff CB: The preeminent role of neuropeptide systems in the early pathophysiology of Alzheimer disease: up with corticotropin-releasing factor, down with acetylcholine. Arch Gen Psychiatry. 1999, 56 (11): 991-2.
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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