=== Genetik ===
Alzheimers og dens relaterede hukommelsesproblemer har en genetisk arvelighed på mellem 49 % og 79 %.<ref name="pmid20930268">{{vcite journal | vauthors = Wilson RS, Barral S, Lee JH |display-authors=etal | title = Heritability of different forms of memory in the Late Onset Alzheimer's Disease Family Study.  | journal = Journal of Alzheimer's Disease | volume = 23 | issue = 2 | pages = 249–55 | year = 2011 | pmid = 20930268 | doi = 10.3233/JAD-2010-101515 }}</ref><ref name="pmid16461860">{{vcite journal | vauthors = Gatz M, Reynolds CA, Fratiglioni L |display-authors=etal |  title = Role of genes and environments for explaining Alzheimer disease  | journal = Arch. Gen. Psychiatry | volume = 63 | issue = 2 | pages = 168–74 | year = 2006 | month = Feb | pmid = 16461860 | doi = 10.1001/archpsyc.63.2.168 }}</ref> Omkring 0,1 % af tilfældene er familiære former for [[autosom]]al (ikke-[[Kønskromosombunden nedarvning|kønsbunden]]) [[Dominansforhold|dominant]] arv, som begynder, før man bliver 65 år.<ref name="pmid16876668">{{vcite journal | vauthors = Blennow K, de Leon MJ, Zetterberg H | title = Alzheimer's Disease | journal = Lancet | volume = 368 | issue = 9533 | pages = 387–403 | year = 2006 | pmid = 16876668 | doi = 10.1016/S0140-6736(06)69113-7 | month = July }}</ref> Denne form af sygdommen kendes som [[Familiær Alzheimers sygdom|tidligt indtrådt, familiær Alzheimers sygdom]]. Størstedelen af tilfælde af autosomal dominant, familiær AD kan tilskrives mutationer i et af tre gener: dem, der koder for [[amyloid-precursor-protein]] (APP) og [[præsenilin]] 1 og 2.<ref name="pmid18332245">{{vcite journal | vauthors = Waring SC, Rosenberg RN | title = Genome-wide association studies in Alzheimer disease | journal = Archives of Neurology | volume = 65 | issue = 3 | pages = 329–34 | year = 2008 | pmid = 18332245 | doi = 10.1001/archneur.65.3.329 | month = March }}</ref> De fleste mutationer i APP- og præsenilin-generne øger produktionen af et lille protein kaldet [[Aβ]]42, som er den centrale komponent i et [[neuritisk plak]].<ref name=Selkoe>{{vcite journal | author = Selkoe DJ | title = Translating cell biology into therapeutic advances in Alzheimer's disease | journal = Nature | volume = 399 | issue = 6738 Suppl | pages = A23–31 | year = 1999 | pmid = 10392577 | doi = 10.1038/19866 | month = June }}</ref> Nogle af mutationerne nøjes med at ændre fordelingen mellem Aβ42 og de andre større former — især Aβ40 — uden at øge mængden af Aβ42.<ref name=Borchelt>{{vcite journal | vauthors = Borchelt DR, Thinakaran G, Eckman CB |display-authors=etal | title = Familial Alzheimer's disease-linked presenilin 1 variants elevate βA1-42/1-40 ratio in vitro and in vivo | journal = Neuron | volume = 17 | issue = 5 | pages = 1005–13 | year = 1996 | pmid = 8938131 | doi = 10.1016/S0896-6273(00)80230-5 |url=http://ac.els-cdn.com/S0896627300802305/1-s2.0-S0896627300802305-main.pdf?_tid=e1a5d3c4-f405-11e4-ac9c-00000aacb362&acdnat=1430926862_7e175593a77c62b8a2646077b6b07ba4 |format=PDF}}</ref><ref name="pmid17254019">{{vcite journal | vauthors = Shioi J, Georgakopoulos A, Mehta P |display-authors=etal | title = FAD mutants unable to increase neurotoxic Aβ 42 suggest that mutation effects on neurodegeneration may be independent of effects on Abeta | journal = Journal of Neurochemistry | volume = 101 | issue = 3 | pages = 674–81 | year = 2007 | pmid = 17254019 | doi = 10.1111/j.1471-4159.2006.04391.x }}</ref>
Videnskab Naturvidenskab