Alzheimer ana (AD) a pathophysiology gaw, n kaja ai protein ni, machyi ai lam ni hte neuron ni a bungli n galaw ai lam ni law wa ai majaw byin ai.
AD a madung kumla lahkawng gaw, amyloid-beta (Aβ) plaques hte neurofibrillary tangles (NFTs) ni nga ai.
Amyloid-beta plaque ngu ai gaw, amyloid precursor protein (APP) hpe enzymes ni hte daw kau nhtawm, Aβ peptide ni byin wa ai shaloi byin wa ai.
Dai peptide ni gaw, n mai hkraw ai fibril ni hpe galaw nna, neuron shinggan de mahkawng nga ai. Dai majaw, cell hte cell matut mahkai lam hten mat nna, neuron ni si mat ai.
Aβ plaque ni law wa ai gaw, AD byin wa ai shawng nnan na lam langai re ai hpe kam ma ai.
Neurofibrillary tangles ngu ai gaw, tau ngu ai protein gaw, hyperphosphorylated byin wa nna, neuron kata hta n kaja ai lam ni byin wa ai shaloi byin wa ai.
Dai zawn gyit hkang ai lam ni gaw, neuron kata hta lusha hte kaga arung arai ni htaw shalai ya na matu ahkyak ai microtubule ni a bungli hpe jahten ya ai.
Dai majaw, dai neuron ni si mat ai.
Ana htang maja ai lam gaw, ana byin ai lam hta mung akyu nga ai.
Immune system gaw Aβ plaques hte NFT ni hpe htang maja ai shaloi pro-inflammatory cytokines ni hpe shapraw ya ai majaw, neuron ni grau sawng wa chye ai.
Dai hta n-ga, oxidative stress, mitochondrial dysfunction, hte glucose metabolism hten ai lam ni gaw AD ana a pathophysiology hpe shabyin ya ai lam ni nga ai.
Dai lam ni gaw, neuron ni n bungli galaw ai hte si mat wa nna, ana grau sawng wa chye ai.
AD ana a lam gaw, ana a majaw chye ginhka ai atsam yawm wa nna, matsing n nga mat hkra byin shangun ai lam ni law law a majaw re.
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.
['N hkap la ai lam: tsi mawan']
['Ndai website gaw hpaji jaw ai hte chye na matu sha galaw da ai.']
['Ndai laika buk hta lawm ai lam ni hpe hkamja lam hte seng nna, ana jep ai (sh) tsi ai lam hta n mai jai lang ai.']
['Ga san ni a mahtai hpe shapraw ya ai neural net gaw, ga shadawn, masha langai ngai hta ana langai ngai mu lu ai lam ni hpe madun ai shaloi, n hkrak ai.']
['Ndai website hta mu lu ai lam ni a majaw, tsi sarawun ni a hpaji jaw ga hpe galoi mung n madat ai sha, hpang hkrat ai lam n galaw u. Tsi hte seng nna, ra kadawn nga ai lam nga yang, 911 hpe shaga u. Ndai website hte dai hpe lang ai lam gaw, tsi sarawun hte machyi masha lapran hku hkau lam n nga ai. BioMedLib hte shi a bungli galaw masha ni, ndai website hta shang lawm ai ni kadai mung, ndai kaw lawm ai shiga hte seng nna, tsun mayu ai lam (sh) tsun ai hku nna, hpa ga sadi jaw ai lam n nga ai.']
['Hti na ahkang n nga ai: copyright']
['1998 ning Digital Millennium Copyright Act, 17 U.S.C. § 512 (the DMCA) gaw Internet kaw mara da ai lam ni gaw US copyright law npu na madu a ahkaw ahkang hpe tawt lai ai ngu kam ai copyright madu ni hpe ahkaw ahkang jaw da ai.']
['Anhte a website hte seng nna, (sh) anhte a magam bungli ni hte seng nna, mara shagun da ai lam ni gaw, na a copyright hpe tawt lai ai ngu nna nang kam ai nga yang, dai lam ni hpe dawm kau na matu (sh) dai ni hpe n mai lu hkra pat kau na matu, nang (sh) na a kasa gaw anhte hpe shana mai ai.']
['Dai shiga ni hpe laika hte ka nna email hte shagun ra ai (email address hpe "Contact" daw kaw mu lu na re).']
['Dai DMCA gaw, na a copyright tawt lai ai lam hpe shana ai hta lawu na lam ni lawm ra ai: (1) tawt lai ai ngu ai copyright lu ai bungli a lam; (2) tawt lai ai ngu ai lam hte seng ai lam hte dai hpe mu tam lu na matu anhte hpe karum ya ai lam; (3) na a matut mahkai lam, na a shara, phone number hte email hte seng ai lam ni; (4) nang mara shagun ai lam gaw copyright madu, shi a agent (sh) tara upadi hte n seng ai ngu ai hpe nang kam ai lam.']
['(5) N teng n man ai sakse hkam ai lam hte seng nna, nang masat da ai hte maren, shana ai lam hta lawm ai shiga ni gaw teng man ai hte, nang tawt lai ai ngu ai copyright hpe hkan sa na ahkang nga ai lam.']
['hte (6) copyright madu a mying hte galaw na ahkang lu ai wa a hkum hkrang (sh) electronic signature.']
['Lahta na lam ni hpe n ka bang ai rai yang, nang shagun ai laika hpe hpang hkrat ai hte n mai htang ai.']
['Matut Mahkai U']
['Gara hku mung san mayu yang email hte shana ya rit.']
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.
['Hkrang']
['BioMedLib gaw ga san hte mahtai yan hpe shapraw na matu computer (machine-learning algorithms) ni hpe lang ai.']
['Anhte gaw PubMed/Medline kaw na tsi hpaji hte seng ai laika buk wan 35 hte hpang ai. RefinedWeb kaw na mung re.']
