Patofysiologiin í Alzheimer sjúku (AD) er ein kompleks prosess, sum hevur við sær upphoping av óvanligum proteinum, inflammatión og nervafunktiónsskaðar.
Tvey høvuðseyðkenni fyri Alzheimer eru, at tað eru amyloid-beta (Aβ) plátur og neurofibrillar tangles (NFT) í heilanum.
Amyloid- beta plátur verða gjørdar, tá ið brot av amyloid precursor proteininum (APP) verða klødd av enzymum til at gera Aβ peptidir.
Hesi peptidir savna seg og mynda óloysilig fibrillir, sum savnast uttanfyri nervakyknurnar, og sum bróta samskiftið millum kyknurnar og elva til deyða á kyknunum.
Hildið verður, at upphópanin av Aβ-plátum er ein av fyrstu hendingunum í menningini av Alzheimer og at hon er við til at fremja ta neurodegenerativu gongdina.
Neurofibrillar tanglar verða gjørdir tá ið proteinið tau verður hyperfosforylerað og ger óvanligar filamentir inni í neuronum.
Hesar fløkjurnar órógva vanliga virksemið hjá mikrotubulunum, sum eru neyðugir fyri at føðsluevni og annað kann flytast í nervakyknuni.
Trupuleikarnir elva til, at nervakyknurnar doyggja.
Inflammatión hevur eisini ein leiklut í patofysiologiini av AD.
Immunskipanin svarar upp á upphópan av Aβ-plátum og NFT við at geva frá sær pro-inflammatorisk cytokine, sum kunnu økja um skaðan á nervakyknurnar.
Harumframt eru prógv fyri, at oxidativur stress, mitochondrial dysfunction, og skert glukose metabolisma eru við til at vera orsøk til sjúkufysiologiina av AD.
Hesi viðurskifti kunnu elva til, at nervakyknurnar ikki virka rætt og doyggja, og harvið versna sjúkugongdin.
Yvirhøvur er patofysiologiin hjá Alzheimer eitt samansett samspæl av fleiri faktorum, sum í síðsta enda elva til stigvísa afturgongd í kognitivu funktiónini og minnisloysi, sum eyðkennir sjúkuna.
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.
['Avsakan: sjúkuviðurskifti']
['Henda heimasíðan er bert til undirvísingar og kunningar og er ikki ætlað sum læknalig ráðgeving ella faklig tænasta.']
['Upplýsingarnar eiga ikki at verða nýttar til at staðfesta ella viðgera nakran heilsutrupulleika ella sjúku, og tey, sum ynskja persónliga læknahjálp, eiga at venda sær til ein autoriseraðan lækna.']
['Gev gætur, at tað neuronala netið, sum gevur svar uppá spurningarnar, er serliga skeivt, tá ið talan er um talgilda innihaldið, t.d. talið av fólki, sum hava fingið staðfest eina ávísa sjúku.']
['Spyr altíð læknan ella annan skikkaðan heilsuhjálpara um ráðgeving í sambandi við sjúku. Vanvirð ongantíð professionella læknaráðgeving ella drála við at leita eftir henni vegna okkurt, tú hevur lisið á hesi heimasíðu.']
['Avsakan: upphavsrættur']
['Digital Millennium Copyright Act frá 1998, 17 U.S.C. § 512 (DMCA) gevur rætt til at kæra til rættindahavarar, sum halda, at tilfar, sum kemur á internetið, brýtur teirra rættindi sambært amerikanskum lógum um upphavsrætt. ']
['Um tú í góðari trúgv heldur, at eitthvørt innihald ella tilfar, sum er gjørt tøkt í sambandi við okkara heimasíðu ella tænastur, brýtur tíni upphavsrættindi, kanst tú (ella tín umboðsmaður) senda okkum eina fráboðan, har tú biður um, at innihaldið ella tilfarið verður tikið burtur ella atgongdin til tað verður sperrað.']
['Tilmeldingarnar skulu verða skrivligar við telduposti (sí "Kontakt" fyri teldupostadressu).']
['DMCA krevur, at fráboðan um meint brot á upphavsrættin skal innihalda hesar upplýsingar: (1) lýsing av tí upphavsrættarliga verkinum, sum talan er um, (2) lýsing av tí meinta brot á upphavsrættin og upplýsingar, sum eru nøktandi til at vit kunnu finna innihaldið (3) upplýsingar um teg, t.d. tín bústað, telefonnummar og teldupostbústað (4) eina váttan frá tær um, at tú í góðari trúgv heldur, at innihaldið, sum tú klagar um, ikki er loyvt av rættindahavanum ella umboði hansara ella sambært lóggávu']
['5) eina váttan frá tær, undirskrivað undir revsing fyri lygi, um, at upplýsingarnar í fráboðanini eru rættar, og at tú hevur heimild at gera galdandi upphavsrættin, sum verður hildin at vera brotin,']
['og 6) fysiska ella elektroniska undirskrift hjá rættindahavara ella persóni, sum hevur loyvi at virka fyri rættindahavara.']
['Um tú ikki hevur upplýst allar omanfyri nevndu upplýsingar, kann tað hava við sær, at viðgerðin av klaguni verður seinkað.']
['Set teg í samband við']
['Vinarliga send okkum ein teldupost við einum hvørjum spurningi/uppskoti.']
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.
['Umleið']
['BioMedLib nýtir sjálvvirkandi teldur (maskinlæringaralgoritmur) til at gera spurningar og svar.']
['Vit byrja við 35 milliónum av biomedicinskum útgávum frá PubMed/Medline. eisini heimasíðum frá RefinedWeb.']
