Editing Down syndrome (section)

==Mechanism==
The extra genetic material present in Down syndrome results in overexpression of a portion of the 310 genes located on chromosome 21.<ref name=Lana2011/> This overexpression has been estimated at 50%, due to the third copy of the chromosome present.<ref name=Nel2010/> Some research has suggested the Down syndrome critical region is located at bands 21q22.1–q22.3,<ref>{{cite web |url=http://emedicine.medscape.com/article/943216-overview |title=Genetics of Down syndrome |access-date=2011-05-29 |url-status=live |archive-url=https://web.archive.org/web/20110527214124/http://emedicine.medscape.com/article/943216-overview |archive-date=2011-05-27 }}</ref> with this area including genes for the [[amyloid precursor protein]], [[superoxide dismutase]], and likely the [[ETS2]] proto [[oncogene]].<ref>{{cite book|title=Current diagnosis & treatment psychiatry|year=2008|publisher=McGraw-Hill Medical|location=New York|isbn=978-0-07-142292-5|pages=Chapter 3|edition=2nd| veditors = Ebert MH |chapter=Psychiatric Genetics}}</ref> Other research, however, has not confirmed these findings.<ref name=Lana2011/> [[MicroRNA]]s are also proposed to be involved.<ref>{{cite journal | vauthors = Patterson D, Cabelof DC | title = Down syndrome as a model of DNA polymerase beta haploinsufficiency and accelerated aging | journal = Mechanisms of Ageing and Development | volume = 133 | issue = 4 | pages = 133–137 | date = April 2012 | pmid = 22019846 | doi = 10.1016/j.mad.2011.10.001 | s2cid = 3663890 }}</ref>

The dementia that occurs in Down syndrome is due to an excess of [[amyloid beta]] [[peptide]] produced in the brain and is similar to [[Alzheimer's disease]], which also involves amyloid beta build-up.<ref name=Wek2013/> Amyloid beta is processed from amyloid precursor protein, the gene for which is located on chromosome 21.<ref name=Wek2013>{{cite journal | vauthors = Weksler ME, Szabo P, Relkin NR, Reidenberg MM, Weksler BB, Coppus AM | title = Alzheimer's disease and Down's syndrome: treating two paths to dementia | journal = Autoimmunity Reviews | volume = 12 | issue = 6 | pages = 670–673 | date = April 2013 | pmid = 23201920 | doi = 10.1016/j.autrev.2012.10.013 }}</ref> [[Senile plaques]] and [[neurofibrillary tangle]]s are present in nearly all by 35&nbsp;years of age, though dementia may not be present.<ref name=Steph2010/> It is hypothesized that those with Down syndrome lack a normal number of [[lymphocytes]] and produce less [[antibody|antibodies]] which is said to present an increased risk of infection.<ref name=Hick2012/>

===Epigenetics===
Down syndrome is associated with an increased risk of some chronic diseases that are typically associated with older age such as Alzheimer's disease. It is believed that accelerated aging occurs and increases the biological age of tissues, but molecular evidence for this hypothesis is sparse. According to a biomarker of tissue age known as [[epigenetic clock]], it is hypothesized that trisomy 21 increases the age of blood and brain tissue (on average by 6.6 years).<ref name="Horvath2015DownSyndrome">{{cite journal | vauthors = Horvath S, Garagnani P, Bacalini MG, Pirazzini C, Salvioli S, Gentilini D, Di Blasio AM, Giuliani C, Tung S, Vinters HV, Franceschi C | display-authors = 6 | title = Accelerated epigenetic aging in Down syndrome | journal = Aging Cell | volume = 14 | issue = 3 | pages = 491–495 | date = June 2015 | pmid = 25678027 | pmc = 4406678 | doi = 10.1111/acel.12325 }}</ref>