{"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\/nb\/arsak-til-alzheimers-sykdom\/","title":{"rendered":"Ny teori fors\u00f8ker \u00e5 forklare \u00e5rsaken til Alzheimers sykdom"},"content":{"rendered":"

Mer enn halvparten av alle demenstilfeller klassifiseres i dag som Alzheimers sykdom - en kronisk nevrodegenerativ sykdom som gradvis p\u00e5virker en persons kognisjon og hukommelse. <\/p>\n\n\n\n

Frem til i dag har man trodd at sykdommen skyldes genetiske faktorer og aldringsfaktorer, og skurkene og hovedskyldige i sykdommen tilskrives senile plakk og nevrofibrill\u00e6r sammenfiltring, som f\u00f8rer til nevroinflammasjon og i neste omgang nevrond\u00f8d. <\/p>\n\n\n\n

However, a new theory of Alzheimer\u2019s disease causes shines a light into the sky of medical research. <\/p>\n\n\n\n

The theory is that genetics and aging are not the only factors responsible for the formation of amyloid clumps \u2013 the protein that accumulates between neurons causing Alzheimer\u2019s disease \u2013 but it can be also a trigger response to microbe infection.  <\/p>\n\n\n\n

La oss se n\u00e6rmere p\u00e5 en nevrologisk skala for \u00e5 forst\u00e5 hele bildet av hva som skjer inne i en hjerne med Alzheimers sykdom. Det er to store fenomener som foreg\u00e5r.<\/p>\n\n\n\n

Proteinet tau er ansvarlig for \u00e5 opprettholde stabiliteten ved \u00e5 gi st\u00f8tte til mikrotubuli inne i nevronene. I en hjerne som lider av tilstanden, er tau biokjemisk modifisert ved en reaksjon som kalles hyperfosforyleringsreaksjon. <\/p>\n\n\n\n

The result of this change is insoluble proteins pieces inside the neuron, breaking down the whole system and killing neuron cells. <\/p>\n\n\n\n

Disse uoppl\u00f8selige bitene av tau-proteiner aggregerer til hverandre og danner den s\u00e5kalte nevrofibrill\u00e6re floker.<\/strong><\/p>\n\n\n

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

Den senile plakk<\/strong> er laget av amyloid-\u03b2-peptider<\/strong>. Et protein som finnes i nevronmembranen (pre-amyloid), gjennomg\u00e5r en spaltningsprosess som resulterer i frie biter av amyloid-\u03b2 utenfor nevronene*. <\/p>\n\n\n\n

Disse bitene skal egentlig renses fra det ytre nevronmediet av spesielle celler og enzymer gjennom fagocytose, men p\u00e5 grunn av genetiske faktorer eller aldringsfaktorer skjer ikke denne prosessen effektivt nok, noe som f\u00f8rer til frie biter av ul\u00f8selige amyloid-\u03b2-proteiner som begynner \u00e5 samle seg til plakk.<\/p>\n\n\n

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

The amyloid plaques are the ones most studied and discussed to be the cause of Alzheimer\u2019s disease. But scientist also affirm the neurofibrillary tangles is directly associated with the disease progression.<\/p>\n\n\n

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

Forskerne fant ogs\u00e5 amyloidklumper i friske, d\u00f8de hjerner. Det betyr at i en frisk gammel hjerne blir ogs\u00e5 renseprosessen mindre effektiv, men ikke like mye som i en hjerne med Alzheimers sykdom.<\/p>\n\n\n\n

Derfor er det et stort antall av disse senile plakk og nevrofibrill\u00e6re floker som kjennetegner Alzheimers sykdom; de blir ekstremt giftige for hjernen og endrer effektiviteten og kvaliteten p\u00e5 synapsene. <\/p>\n\n\n\n

Subjects affected show symptoms like memory loss, confusion related to time and location, depression, anxiety, language and communication problems, mood instability, and others.<\/p>\n\n\n\n

I den nye foresl\u00e5tte teorien<\/strong>er de amyloide plakk en mekanisme for \u00e5 beskytte hjernen mot mikrobeinfeksjoner. <\/p>\n\n\n\n

Amyloid-\u03b2-genet finnes i en stor del av virveldyrgruppen, og det har blitt bevart p\u00e5 tvers av ulike arter i flere generasjoner, noe som betyr at det b\u00f8r ha en nyttig og viktig rolle for kroppen v\u00e5r, og ikke bare fungere som noe skadelig - hvis det ikke var noe verdifullt eller fordelaktig, ville genet ha blitt borte for lenge siden gjennom evolusjonen.<\/p>\n\n\n\n

Forskerne gikk l\u00f8s p\u00e5 tusenvis av obduserte hjerner fra personer med Alzheimers sykdom. <\/p>\n\n\n\n

Although they faced difficulties in analyzing these types of brain due to bad condition, they were able to study and collect information to later propose a few possible microbes\u2019 triggers. <\/p>\n\n\n\n

Disse utl\u00f8serne er forsvarsmekanismer mot noen typer humane herpesvirus, som herpesvirus 1, 6A og 7, og tre bakterier, Chlamydia pneumonia<\/em>, Borrelia burgdorferi<\/em>, Porphyromonas gingivalis<\/em>.<\/p>\n\n\n\n

Teorien er at beta-amyloid i utgangspunktet har en defensiv funksjon ved \u00e5 fange opp mikrober som beveger seg mot hjernen, og dermed stoppe en eventuell infeksjon eller sykdom. <\/p>\n\n\n\n

Som nevnt mister hjernen p\u00e5 grunn av aldringsfaktorer sin evne til effektivt \u00e5 rense amyloidene. Dermed kan ideen om amyloidets funksjon v\u00e6re feil hele tiden; det er sannsynligvis involvert i en type antimikrobiell beskyttelse mot inntrengere i hjernen, og er klassifisert som et antimikrobielt peptid.<\/p>\n\n\n\n

Forskere har f\u00e5tt positive resultater n\u00e5r de har fors\u00f8kt \u00e5 p\u00e5vise at \u03b2-amyloid kan drepe mikroorganismer fra noen vanlige sykdommer. <\/p>\n\n\n\n

En annen studie som startet i 2007 og som skal avsluttes i 2022 ved Columbia-universitetet i New York, tester et antiviralt medikament p\u00e5 pasienter med h<\/s>erpes simplex-virus 1 og mild Alzheimers sykdom, for \u00e5 se om medikamentet kan bremse sykdomsutviklingen. <\/p>\n\n\n\n

Forel\u00f8pig kan vi bare h\u00e5pe p\u00e5 det beste og vente p\u00e5 resultatene.<\/p>\n\n\n\n

This new proposed theory is still not well accepted by all scientific community. Many scientists argue that even if this new proposed theory comes to be proven, genetic factors and bad mutations are still going to be the main cause of the disease. <\/p>\n\n\n\n

Alzheimer’s disease is still a condition with very little scientific knowledge of its real causes; there is no cure and not many therapeutic treatment options. If this theory ended to be true, it could be the first step in the direction of better treatments. Go science!<\/p>\n\n\n\n

Referanser<\/strong><\/p>\n\n\n\n

ABBOTT, A. Er infeksjoner grobunn for noen tilfeller av Alzheimers sykdom? Natur<\/strong>, v. 587, nr. 7832, s. 22-25, 4. nov. 2020.<\/p>\n\n\n\n

CEC\u00cd, K. et al. Biomarkers in Alzheimer disease. Geriatri, gerontologi og aldring<\/strong>, v. 6, nr. 3, s. 273-282, 2012.<\/p>\n\n\n\n

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

YOO, K.-Y.; PARK, S.-Y. Terpenoider som potensielle legemidler mot Alzheimers sykdom. Molekyler<\/strong>, v. 17, nr. 3, s. 3524-3538, mar. 2012.<\/p>\n\n\n\n

___
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Mer enn halvparten av alle demenstilfeller klassifiseres i dag som Alzheimers sykdom - en kronisk nevrodegenerativ sykdom som gradvis p\u00e5virker en persons kognisjon og hukommelse. Frem til i dag har man trodd at sykdommen skyldes genetiske faktorer og aldringsfaktorer, mens skurkene og de viktigste \u00e5rsakene til sykdommen tilskrives [...].<\/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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