Altsgeymer kasalligining patofiziologiyasi (AD) g'ayritabiiy oqsillar to'planishi, yallig'lanish va neyronlar funktsiyasi buzilishini o'z ichiga olgan murakkab jarayondir.
ADning ikkita asosiy belgisi miyada amiloid-beta (Aβ) plaklari va neyrofibrillar to'qnashuvlar (NFT) mavjudligi hisoblanadi.
Amiloid- beta plaklar amiloid prekursor oqsilining (APP) parchalari Aβ peptidlarini hosil qilish uchun fermentlar tomonidan bo'linib ketganda hosil bo'ladi.
Ushbu peptidlar to'planib, neyronlar tashqarisida to'planadigan erimaydigan fibrillalarni hosil qiladi, bu esa hujayralar o'rtasidagi aloqani buzadi va neyronlarning o'limiga olib keladi.
Aβ plakalarining to'planishi AD rivojlanishining dastlabki hodisalaridan biri deb hisoblanadi va u neyrodegenerativ jarayonga hissa qo'shadi deb ishoniladi.
Neurofibrillar to'qnashuvlar tau oqsili giperfosforillanganida va neyronlar ichida g'ayrioddiy filamentlar hosil bo'lganda hosil bo'ladi.
Ushbu to'qnashuvlar neyron ichidagi ozuqa moddalari va boshqa materiallarni tashish uchun zarur bo'lgan mikrotubulalarning normal ishlashini buzadi.
Bu to'qnashuvlar oxir-oqibat zarar ko'rgan neyronlarning o'limiga olib keladi.
Yallig'lanish, shuningdek, ADning patofiziologiyasida ham rol o'ynaydi.
Immunitet tizimi Aβ plaklari va NFTlarning to'planishiga yallig'lanishni oldini oluvchi sitokinlarni chiqarib yuborish orqali javob beradi, bu esa neyronlarga yetkazilgan zararni kuchaytirishi mumkin.
Bundan tashqari, oksidatsion stress, mitoxondriya disfunktsiyasi va glyukoza metabolizmining buzilishi ADning patofiziologiyasiga hissa qo'shishi haqida dalillar mavjud.
Ushbu omillar neyronlarning funktsiyasi buzilishiga va o'limiga olib kelishi mumkin, bu esa kasallik jarayonini yanada kuchaytiradi.
Umuman olganda, ADning patofiziologiyasi ko'plab omillarning murakkab o'zaro ta'siri bo'lib, oxir-oqibat kasallikka xos bo'lgan kognitiv funktsiyaning asta-sekin pasayishiga va xotira yo'qolishiga olib keladi.
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.
Mas'uliyatdan voz kechish: tibbiy
Ushbu veb-sayt faqat ta'lim va axborot maqsadlari uchun mo'ljallangan bo'lib, tibbiy maslahat yoki professional xizmatlar ko'rsatmaydi.
Ma'lumotlardan sog'liqni saqlash muammolari yoki kasalliklarni tashxislash yoki davolash uchun foydalanmaslik kerak va shaxsiy tibbiy maslahat so'raganlar litsenziyaga ega bo'lgan shifokor bilan maslahatlashishlari kerak.
Iltimos, savollarga javoblarni ishlab chiqaradigan neyron tarmog'i, ayniqsa, raqamli tarkibga kelganda noto'g'ri ekanligiga e'tibor bering. Masalan, ma'lum bir kasallik bilan kasallangan odamlar soni.
Har doim shifokoringiz yoki boshqa malakali sog'liqni saqlash provayderining maslahatini so'rang. Hech qachon professional tibbiy maslahatni e'tiborsiz qoldirmang yoki ushbu veb-saytda o'qiganingiz sababli uni so'rashni kechiktirmang. Agar siz tibbiy favqulodda vaziyatga duchor bo'lishingiz mumkin deb o'ylasangiz, darhol 911 ga qo'ng'iroq qiling yoki eng yaqin favqulodda vaziyatlar bo'limiga boring. Ushbu veb-sayt yoki uning ishlatilishi bilan hech qanday shifokor- bemor munosabatlari yaratilmaydi. BioMedLib ham, uning xodimlari ham, ushbu veb-saytga hech qanday hissa qo'shuvchi, bu erda taqdim etilgan ma'lumot yoki uning ishlatilishi bilan bog'liq hech qanday bayonot bermaydi.
Mas'uliyatdan voz kechish: mualliflik huquqi
1998-yilgi raqamli ming yillik mualliflik huquqi to'g'risidagi qonun, 17 U.S.C. 512-moddasi (DMCA) Internetda paydo bo'lgan materiallar AQSh mualliflik huquqi to'g'risidagi qonun bo'yicha o'z huquqlarini buzadi deb hisoblaydigan mualliflik huquqi egalari uchun choralar ko'rsatadi.
Agar siz bizning veb-saytimiz yoki xizmatlarimiz bilan bog'liq bo'lgan har qanday tarkib yoki material sizning mualliflik huquqingizni buzadi deb yaxshi ishonchga ega bo'lsangiz, siz (yoki sizning vakilingiz) bizga tarkib yoki materialni olib tashlashni yoki unga kirishni to'xtatishni so'rab xabar yuborishingiz mumkin.
Xabarlar yozma ravishda elektron pochta orqali yuborilishi kerak (elektron pochta manzili uchun "Muloqot" bo'limiga qarang).
DMCA sizning da'vo qilingan mualliflik huquqi buzilganligi to'g'risidagi xabarnomangizda quyidagi ma'lumotlarni o'z ichiga olishini talab qiladi: (1) da'vo qilingan mualliflik huquqi buzilgan asarning tavsifi; (2) da'vo qilingan mualliflik huquqi buzilgan tarkibning tavsifi va bizga tarkibni topishga imkon beradigan etarli ma'lumotlar; (3) siz uchun aloqa ma'lumotlari, shu jumladan sizning manzilingiz, telefon raqami va elektron pochta manzili; (4) siz tomonidan da'vo qilingan tarzda tarkib mualliflik huquqi egasi yoki uning vakili yoki har qanday qonun tomonidan ruxsat berilmaganligiga ishonchingiz borligi to'g'risidagi bayonot;
(5) siz tomonidan yolg'on guvohlik berish jazosi ostida imzolangan, bildirishnomadagi ma'lumotlar to'g'ri ekanligi va siz buzilgan deb da'vo qilingan mualliflik huquqlarini amalga oshirish vakolatiga ega ekanligingiz to'g'risidagi bayonot;
va (6) mualliflik huquqi egasining yoki mualliflik huquqi egasi nomidan harakat qilishga vakolatli shaxsning jismoniy yoki elektron imzosi.
Yuqoridagi barcha ma'lumotlarni kiritmaslik sizning shikoyatingizni ko'rib chiqishni kechiktirishi mumkin.
Aloqa qilish
Iltimos, har qanday savol / taklif bilan bizga elektron pochta xabarini yuboring.
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.
Disclaimer: medical
This web site is provided for educational and informational purposes only and does not constitute providing medical advice or professional services.
The information provided should not be used for diagnosing or treating a health problem or disease, and those seeking personal medical advice should consult with a licensed physician.
Please note the neural net that generates answers to the questions, is specially inaccurate when it comes to numeric content. For example, the number of people diagnosed with a specific disease.
Always seek the advice of your doctor or other qualified health provider regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. If you think you may have a medical emergency, call 911 or go to the nearest emergency room immediately. No physician-patient relationship is created by this web site or its use. Neither BioMedLib nor its employees, nor any contributor to this web site, makes any representations, express or implied, with respect to the information provided herein or to its use.
Disclaimer: copyright
The Digital Millennium Copyright Act of 1998, 17 U.S.C. § 512 (the “DMCA”) provides recourse for copyright owners who believe that material appearing on the Internet infringes their rights under U.S. copyright law. If you believe in good faith that any content or material made available in connection with our website or services infringes your copyright, you (or your agent) may send us a notice requesting that the content or material be removed, or access to it blocked. Notices must be sent in writing by email (see 'Contact' section for email address) . The DMCA requires that your notice of alleged copyright infringement include the following information: (1) description of the copyrighted work that is the subject of claimed infringement; (2) description of the alleged infringing content and information sufficient to permit us to locate the content; (3) contact information for you, including your address, telephone number and email address; (4) a statement by you that you have a good faith belief that the content in the manner complained of is not authorized by the copyright owner, or its agent, or by the operation of any law; (5) a statement by you, signed under penalty of perjury, that the information in the notification is accurate and that you have the authority to enforce the copyrights that are claimed to be infringed; and (6) a physical or electronic signature of the copyright owner or a person authorized to act on the copyright owner’s behalf. Failure to include all of the above information may result in the delay of the processing of your complaint.
Taxminan
BioMedLib savol-javob juftliklarini yaratish uchun avtomatlashtirilgan kompyuterlardan (mashinani o'rganish algoritmlaridan) foydalanadi.
Biz PubMed/Medline-ning 35 million biomedikal nashrlaridan boshlaymiz. Shuningdek, RefinedWeb-ning veb-sahifalari.
"Referensiyalar"ga shuningdek "Hujjatdan voz kechish"ga qarang.
