{"id":12121,"date":"2021-01-11T11:05:53","date_gmt":"2021-01-11T13:05:53","guid":{"rendered":"https:\/\/mindthegraph.com\/blog\/?p=12121"},"modified":"2023-01-05T14:52:03","modified_gmt":"2023-01-05T17:52:03","slug":"cause-of-alzheimers-disease","status":"publish","type":"post","link":"https:\/\/mindthegraph.com\/blog\/da\/arsag-til-alzheimers-sygdom\/","title":{"rendered":"Ny teori fors\u00f8ger at forklare \u00e5rsagen til Alzheimers sygdom"},"content":{"rendered":"

Mere end halvdelen af tilf\u00e6ldene af demens i dag klassificeres som Alzheimers sygdom - en kronisk neurodegenerativ sygdom, der gradvist p\u00e5virker en persons kognition og hukommelse. <\/p>\n\n\n\n

Indtil i dag har man troet, at sygdommen skyldtes genetiske faktorer og aldring, og skurkene og de st\u00f8rste syndere tilskrives de senile plaques og de neurofibrill\u00e6re sammenfiltringer, som f\u00f8rer til neuroinflammation og i sidste ende neurond\u00f8d. <\/p>\n\n\n\n

Men en ny teori om \u00e5rsagerne til Alzheimers sygdom skinner et lys p\u00e5 den medicinske forsknings himmel. <\/p>\n\n\n\n

Teorien er, at genetik og aldring ikke er de eneste faktorer, der er ansvarlige for dannelsen af amyloidklumper - det protein, der akkumuleres mellem neuroner og for\u00e5rsager Alzheimers sygdom - men det kan ogs\u00e5 v\u00e6re en udl\u00f8sende reaktion p\u00e5 mikrobeinfektion.  <\/p>\n\n\n\n

Lad os se n\u00e6rmere p\u00e5 en neurologisk skala for at forst\u00e5 hele billedet af, hvad der sker inde i en hjerne med Alzheimers sygdom. Der foreg\u00e5r to store f\u00e6nomener.<\/p>\n\n\n\n

Et protein kaldet tau er ansvarligt for at opretholde stabiliteten ved at st\u00f8tte mikrotubuli inde i neuronerne. I en hjerne, der lider af sygdommen, er tau biokemisk modificeret ved en reaktion, der kaldes hyperfosforylatreaktion. <\/p>\n\n\n\n

Resultatet af denne \u00e6ndring er uopl\u00f8selige proteinstykker inde i neuronen, som nedbryder hele systemet og dr\u00e6ber neuroncellerne. <\/p>\n\n\n\n

Disse uopl\u00f8selige stykker af tau-proteiner samler sig til hinanden og danner neurofibrill\u00e6re sammenfiltringer.<\/strong><\/p>\n\n\n

\n
\"\"<\/a><\/figure><\/div>\n\n\n

Den senile plaques<\/strong> er lavet af amyloid-\u03b2-peptider<\/strong>. Et protein, der findes i neuronernes membraner (pr\u00e6amyloid), underg\u00e5r en spaltningsproces, der resulterer i frie stykker af amyloid-\u03b2 uden for neuronerne*. <\/p>\n\n\n\n

Disse stykker skulle egentlig renses fra det ydre neuronmedium af s\u00e6rlige celler og enzymer gennem fagocytose, men p\u00e5 grund af genetiske eller aldringsm\u00e6ssige faktorer sker denne proces ikke effektivt nok, hvilket f\u00f8rer til frie stykker af uopl\u00f8selige amyloid-\u03b2-proteiner, der begynder at samle sig til plaques.<\/p>\n\n\n

\n
\"\"<\/a><\/figure><\/div>\n\n\n

De amyloide plaques er dem, der er mest unders\u00f8gt og diskuteret som \u00e5rsag til Alzheimers sygdom. Men forskere bekr\u00e6fter ogs\u00e5, at de neurofibrill\u00e6re sammenfiltringer er direkte forbundet med sygdommens progression.<\/p>\n\n\n

\n
\"\"<\/a><\/figure><\/div>\n\n\n

Forskerne fandt ogs\u00e5 amyloidklumper i raske post mortem-hjerner. Det betyder, at i en sund gammel hjerne bliver reng\u00f8ringsprocessen ogs\u00e5 mindre effektiv, men ikke s\u00e5 meget som i en hjerne med Alzheimers sygdom.<\/p>\n\n\n\n

Derfor er et stort antal af disse senile plaques og neurofibrill\u00e6re tangles det, der karakteriserer Alzheimers sygdom; de bliver ekstremt giftige for hjernen og \u00e6ndrer synapsernes effektivitet og kvalitet. <\/p>\n\n\n\n

De ramte personer viser symptomer som hukommelsestab, forvirring i forhold til tid og sted, depression, angst, sprog- og kommunikationsproblemer, ustabilt hum\u00f8r og meget andet.<\/p>\n\n\n\n

I den nye foresl\u00e5ede teori<\/strong>If\u00f8lge forskerne er de amyloide plaques en mekanisme, der beskytter hjernen mod mikrobeinfektioner. <\/p>\n\n\n\n

Amyloid-\u03b2-genet findes i en stor del af hvirveldyrsgruppen, og det er blevet bevaret p\u00e5 tv\u00e6rs af forskellige arter i flere generationer, hvilket betyder, at det b\u00f8r have en nyttig og vigtig rolle for vores krop og ikke kun fungere som noget skadeligt - hvis det ikke var noget gyldigt eller gavnligt, ville genet v\u00e6re forsvundet for l\u00e6nge siden gennem den evolution\u00e6re vej.<\/p>\n\n\n\n

Forskere gik efter tusindvis af post mortem-hjerner fra mennesker med Alzheimers sygdom. <\/p>\n\n\n\n

Selvom de havde sv\u00e6rt ved at analysere denne type hjerne p\u00e5 grund af de d\u00e5rlige forhold, var de i stand til at studere og indsamle information for senere at foresl\u00e5 et par mulige mikrobeudl\u00f8sere. <\/p>\n\n\n\n

Disse udl\u00f8sere er forsvarsmekanismer mod nogle typer af humane herpesvirus som herpesvirus 1, 6A og 7 og tre bakterier, Klamydia-lungebet\u00e6ndelse<\/em>, Borrelia burgdorferi<\/em>, Porphyromonas gingivalis<\/em>.<\/p>\n\n\n\n

Teorien er, at beta-amyloid i f\u00f8rste omgang har en defensiv funktion, hvor det fanger de mikrober, der bev\u00e6ger sig mod hjernen, og stopper en mulig infektion eller sygdom. <\/p>\n\n\n\n

Som n\u00e6vnt mister hjernen sin evne til effektivt at rense amyloiderne p\u00e5 grund af aldringsfaktorer. Ideen om amyloidets funktion kan derfor v\u00e6re forkert hele tiden; det er sandsynligvis involveret i en form for antimikrobiel beskyttelse mod hjernens indtr\u00e6ngere, idet det klassificeres som et antimikrobielt peptid.<\/p>\n\n\n\n

Forskere har opn\u00e5et positive resultater i fors\u00f8get p\u00e5 at p\u00e5vise, at \u03b2-amyloid kan dr\u00e6be mikroorganismer fra f\u00e5 almindelige sygdomme. <\/p>\n\n\n\n

Derudover tester et andet studie, der startede i 2007 og forventes afsluttet i 2022 p\u00e5 University of Columbia i New York, et antiviralt l\u00e6gemiddel i patienter med h<\/s>erpes simplex virus 1 og mild Alzheimers sygdom for at se, om l\u00e6gemidlet kan bremse sygdommens udvikling. <\/p>\n\n\n\n

Indtil videre er det eneste, vi kan g\u00f8re, at h\u00e5be p\u00e5 det bedste og vente p\u00e5 resultaterne.<\/p>\n\n\n\n

Denne nye foresl\u00e5ede teori er stadig ikke accepteret af hele det videnskabelige samfund. Mange forskere h\u00e6vder, at selv hvis denne nye teori bliver bevist, vil genetiske faktorer og d\u00e5rlige mutationer stadig v\u00e6re hoved\u00e5rsagen til sygdommen. <\/p>\n\n\n\n

Alzheimers sygdom er stadig en tilstand med meget lidt videnskabelig viden om dens egentlige \u00e5rsager; der er ingen kur og ikke mange terapeutiske behandlingsmuligheder. Hvis denne teori ender med at v\u00e6re sand, kan det v\u00e6re det f\u00f8rste skridt i retning af bedre behandlinger. Kom s\u00e5, videnskab!<\/p>\n\n\n\n

Referencer<\/strong><\/p>\n\n\n\n

ABBOTT, A. Er infektioner grobund for nogle tilf\u00e6lde af Alzheimers sygdom? Natur<\/strong>, v. 587, n. 7832, s. 22-25, 4 nov. 2020.<\/p>\n\n\n\n

CEC\u00cd, K. et al. Biomark\u00f8rer i Alzheimers sygdom. Geriatri, gerontologi og aldring<\/strong>, v. 6, n. 3, s. 273-282, 2012.<\/p>\n\n\n\n

MAKIN, S. Amyloidhypotesen p\u00e5 pr\u00f8ve. Natur<\/strong>, v. 559, n. 7715, p. S4-S7, 25 jul. 2018.<\/p>\n\n\n\n

YOO, K.-Y.; PARK, S.-Y. Terpenoider som potentielle terapeutika mod Alzheimers sygdom. Molekyler<\/strong>, v. 17, n. 3, s. 3524-3538, mar. 2012.<\/p>\n\n\n\n

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Mere end halvdelen af tilf\u00e6ldene af demens klassificeres i dag som Alzheimers sygdom - en kronisk neurodegenerativ sygdom, der gradvist p\u00e5virker en persons kognition og hukommelse. Indtil i dag troede man, at sygdommen skyldtes genetiske og aldringsm\u00e6ssige faktorer, men nu tilskrives skurkene og de vigtigste skyldige i sygdommen [...]<\/p>","protected":false},"author":4,"featured_media":12125,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":[],"categories":[959,28],"tags":[213,554,964,136],"yoast_head":"\nNew Theory Tries to Explain The Cause of Alzheimer\u2019s<\/title>\n<meta name=\"description\" content=\"Read this blog that discusses a new theory that tries to explain the cause of Alzheimer\u2019s disease. 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