What is pathophysiology of Alzheimer?

['ڤڠاجين ڤاسڠ اين']

اڤاكه ڤاتوڤيسيوولوڬي الزهايمر؟

ڤاتوڤيسيوولوڬي كاءداءن الزهايمر (AD) اداله ڤروسيس كومڤليك سڠ مڠاندوڠي ڤمبڠكڠ ڤروتين نانورمال، ڤمباڠونن، وان ديسفڠكسي نورون.

Dua ciri utama AD adalah adanya plak amyloid-beta (Aβ) dan kusut neurofibrillary (NFT) di otak.

ڤلاك ايميولويد-بيتا تله دڤامبڠكن كتيک ڤريڬمن ڤروتين ڤريكورسور ايميولويد (APP) دڤاسڠ اوليه اينزايم اونتوق ممبنتو ڤڤتيد Aβ.

ڤيڤتيد اين ماجوڠ وان ممبنتو فيبريل نڠ تيدق بوليه دڤڠڬوناكن نڠ ماجوڠ د لوار نيورون، ماڠڬڠڬوڠكن كومونيكاسي سيل-كڤد-سيل وان ماجوڠكن كمواتن نيورون.

ڤڠumpulan plak Aβ dianggap sabagai salah satu peristiwa paling awal dalam perkembangan AD, dan dipercayai berkontribusi pada proses neurodegeneratif.

ڤڠڬڠڬوان نيروفيبريلري دڤامبڠكن كتيک ڤروتين تاو منجادي هيبرفوسفوريلات دان ممبنتو فيلامن نانورمال دالم نيورون.

ڤڠڬونجوڠ اين مڠڬونجوڠكن ڤڠڬوناان نورمال ميكروتوبول، نڠ ڤنتيڠ اونتوق ڤڠڬونجوڠ ڤڠهادڤن نوتريين وان ماتريال لاين دالم نورون.

ڤڠڬڠڬوان اخيرڽ ممباوا ك موت نيرون يڠ دتاڠڬوڠي.

ڤنوليسن جوڬ ممڤوڽاءي ڤرلو دالم ڤاتوڤيسيوولوڬي AD.

sistim imun mananggapi panumpuan plak Aβ wan NFT lawan malapasakan sitokin pro-inflamasi, nang kawa maningkatakan karusakan neuron.

سلاين ايت، اد كادا-كادا ڤڠاهاسن نڠ مڠاندوڠي ستريس اوكسيداتيف، ڤڠڬوناكن ميتوچوندريا، وان ميتابوليسمى ڬلوكوز نڠ دتاهن ممباوا كڤد ڤاتوفيزيولوڬي AD.

فاكتور-فاكتور ngini kawa mambawai ka disfungsi wan kamatian neuron, labih maningkatakan proses panyakit.

Secara keseluruhan, patofisiologi AD adalah interaksi kompleks dari beberapa faktor yang akhirnya mengarah pada penurunan progresif fungsi kognitif dan kehilangan memori yang menjadi ciri khas penyakit.

['ڤرودوک']

PubMed/Medline https://www.nlm.nih.gov/databases/download/pubmed_medline.html

RefinedWeb https://arxiv.org/abs/2306.01116

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.

Skoog I, Kalaria RN, Breteler MM: Vascular factors and Alzheimer disease. Alzheimer Dis Assoc Disord. , 13 Suppl 3 (): S106-14.

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.

Raskind MA, Peskind ER: Neurobiologic bases of noncognitive behavioral problems in Alzheimer disease. Alzheimer Dis Assoc Disord. 1994, 8 Suppl 3 (): 54-60.

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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['اڤابيلا ديري سايڠ ڤرچاي اڤاڽ ڤڠاجين اتاو ماتريال يڠ دڤرچاياکن دالم ڤڠڬوناان ويب اتاو ڤرخدمتن ساي مڠهادڤي حق ڤنوليسن ديري، ديري (اتاو ڤڠاجين ديري) بوليه مڠوروسكن ساتو ڤڠاتوسن مڠمبيل ڤڠاجين اتاو ماتريال ايت دڤنوليس اتاو ڤڠاجين ايت دڤنوليس. ']

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['DMCA ممرلوكن ڤڠاجرن ڤڠهيناان حق ڤنوليسن مڠاندوڠي معلومت يڠ تليتي: (1) ڤنوليسن كراجا?? ن حق ڤنوليسن يڠ منجادي موضوع ڤڠهيناان مڠاندوڠي؛ (2) ڤنوليسن كونتين يڠ مڠهيناان ڤنوليسن دان معلومت يڠ كافي اونتوق ممبريكن كيت ڤڠاجرن كونتين؛ (3) معلومت ڤڠاتوهن كيت، ترماسوق ادريس، نومبر تيليفون دان ادريس ايميل كيت؛ (4) ڤڠاجرن كيت يڠ ممڤوڽاءي كيت برهارڤ ڤڠاجرن يڠ دڤنوليسكن تيدق دأوتوريساسي اوليه ڤملكن حق ڤنوليسن، اتاو اڬينڽ، اتاو اوليه ڤڠاجرن ڤرنه.']

['(5) بيانيه اي از طرف شما، با امضاي شما تحت مجازات شهادت دروغين، که اطلاعات در اطلاعيه دقيق است و شما اختيار داريد حقوق كپي رايت را كه ادعا مي شود نقض شده است، اجرا كنيد؛']

['ڠڬوناكن ڤڠڬوناءن حق ڤنوليس اتاو اورڠ يڠ دڤرلوكن اونتوق مڠڬوناكن ڤڠڬوناءن حق ڤنوليس.']

['ڤڠاديلن ممباوا سموا معلومت يڠ دڤرتوان اڤابيلا ممباوا ڤڠاجرن كڤد ڤمبلاجرن.']

['ڤرتامڤوان']

['Tulung kirimi kami surel dengan apa jua pertanyaan/cadangan.']

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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