Editing Human genetic enhancement (section)

=== Behavior ===
{{Further|Behavioural genetics|Genetics of aggression}}

Significant [[Quantitative genetics|quantitative genetic]] discoveries were made in the 1970s and 1980s, going beyond estimating heritability. However, issues such as [[The Bell Curve]] resurfaced, and by the 1990s, scientists recognized the importance of [[genetics]] for behavioral traits such as [[intelligence]]. The [[American Psychological Association]]'s Centennial Conference in 1992 chose [[Behavioural genetics|behavioral genetics]] as a theme for the past, present, and future of [[psychology]]. [[Molecular genetics]] synthesized, resulting in the [[DNA]] revolution and behavioral [[genomics]], as [[Quantitative genetics|quantitative genetic]] discoveries slowed. Individual behavioral differences can now be predicted early thanks to the [[Behavioural sciences|behavioral sciences']] DNA revolution. The first law of behavioral genetics was established in 1978 after a review of thirty twin studies revealed that the average heritability estimate for intelligence was 46%.<ref>{{cite journal | vauthors = Plomin R | title = Celebrating a Century of Research in Behavioral Genetics | journal = Behavior Genetics | volume = 53 | issue = 2 | pages = 75–84 | date = March 2023 | pmid = 36662387 | pmc = 9922236 | doi = 10.1007/s10519-023-10132-3 }}</ref> [[Behavior]] may also be modified by genetic intervention.<ref>{{cite journal | vauthors = Lupton ML | title = Behaviour modification by genetic intervention--the law's response | journal = Medicine and Law | volume = 13 | issue = 5–6 | pages = 417–431 | date = 1994 | pmid = 7845173 }}</ref>  Some people may be aggressive, selfish, and may not be able to function well in society. Mutations in GLI3 and other patterning genes have been linked to HH etiology, according to genetic research. Approximately 50%-80% of children with HH have acute wrath and violence, and the majority of patients have externalizing problems. Epilepsy may be preceded by behavioral instability and intellectual incapacity.<ref>{{cite journal | vauthors = Cohen NT, Cross JH, Arzimanoglou A, Berkovic SF, Kerrigan JF, Miller IP, Webster E, Soeby L, Cukiert A, Hesdorffer DK, Kroner BL, Saper CB, Schulze-Bonhage A, Gaillard WD | display-authors = 6 | title = Hypothalamic Hamartomas: Evolving Understanding and Management | journal = Neurology | volume = 97 | issue = 18 | pages = 864–873 | date = November 2021 | pmid = 34607926 | pmc = 8610628 | doi = 10.1212/WNL.0000000000012773 }}</ref> There is currently research ongoing on genes that are or may be (in part) responsible for selfishness (e.g. [[ruthlessness gene]]), aggression (e.g. [[warrior gene]]), altruism (e.g. [[OXTR]], [[CD38]], [[COMT]], [[DRD4]], [[DRD5]], [[IGF2]], [[GABRB2]]<ref>{{cite journal | vauthors = Thompson GJ, Hurd PL, Crespi BJ | title = Genes underlying altruism | journal = Biology Letters | volume = 9 | issue = 6 | pages = 20130395 | date = 23 December 2013 | pmid = 24132092 | pmc = 3871336 | doi = 10.1098/rsbl.2013.0395 }}</ref>)

There has been a great anticipation of [[Genetic engineering|gene editing]] technology to modify genes and regulate our [[biology]] since the invention of recombinant DNA technology. These expectations, however, have mostly gone unmet. Evaluation of the appropriate uses of germline interventions in reproductive medicine should not be based on concerns about enhancement or eugenics, despite the fact that gene editing research has advanced significantly toward clinical application.<ref>{{cite journal | vauthors = Cwik B | title = Moving Beyond 'Therapy' and 'Enhancement' in the Ethics of Gene Editing | journal = Cambridge Quarterly of Healthcare Ethics | volume = 28 | issue = 4 | pages = 695–707 | date = October 2019 | pmid = 31526421 | pmc = 6751566 | doi = 10.1017/S0963180119000641 }}</ref>

[[Cystic Fibrosis (CF)|Cystic fibrosis (CF)]] is a [[hereditary disease]] caused by mutations in the [[Cystic fibrosis transmembrane conductance regulator|Cystic fibrosis transmembrane conductance regulator (CFTR)]] gene. While 90% of CF patients can be treated, current treatments are not curative and do not address the entire spectrum of CFTR mutations. Therefore, a comprehensive, long-term therapy is needed to treat all [[Cystic fibrosis|CF]] patients once and for all. [[CRISPR/Cas]] [[Genetic engineering|gene editing]] technologies are being developed as a viable platform for genetic treatment.<ref>{{cite journal | vauthors = Wang G | title = Genome Editing for Cystic Fibrosis | journal = Cells | volume = 12 | issue = 12 | page = 1555 | date = June 2023 | pmid = 37371025 | pmc = 10297084 | doi = 10.3390/cells12121555 | doi-access = free }}</ref> However, the difficulties of delivering enough [[CFTR (gene)|CFTR gene]] and sustaining expression in the lungs has hampered gene therapy's efficacy. Recent technical breakthroughs, including as [[Viral vector|viral]] and non-viral vector transport, alternative [[nucleic acid]] technologies, and new technologies like [[mRNA]] and [[CRISPR gene editing]], have taken use of our understanding of [[Cystic fibrosis|CF]] biology and airway epithelium.<ref>{{cite journal | vauthors = Allen L, Allen L, Carr SB, Davies G, Downey D, Egan M, Forton JT, Gray R, Haworth C, Horsley A, Smyth AR, Southern KW, Davies JC | display-authors = 6 | title = Future therapies for cystic fibrosis | journal = Nature Communications | volume = 14 | issue = 1 | pages = 693 | date = February 2023 | pmid = 36755044 | pmc = 9907205 | doi = 10.1038/s41467-023-36244-2 | bibcode = 2023NatCo..14..693A }}</ref>

Human [[gene transfer]] has held the promise of a lasting remedy to hereditary illnesses such as [[Cystic Fibrosis (CF)|cystic fibrosis (CF)]] since its conception and use. The emergence of sophisticated technologies that allow for site-specific alteration with programmable nucleases has greatly revitalized the area of [[gene therapy]].<ref>{{cite journal | vauthors = Maule G, Arosio D, Cereseto A | title = Gene Therapy for Cystic Fibrosis: Progress and Challenges of Genome Editing | journal = International Journal of Molecular Sciences | volume = 21 | issue = 11 | page = 3903 | date = May 2020 | pmid = 32486152 | pmc = 7313467 | doi = 10.3390/ijms21113903 | doi-access = free }}</ref> There is some research going on on the [[hypothetical]] treatment of psychiatric disorders by means of gene therapy. It is assumed that, with gene-transfer techniques, it is possible (in experimental settings using animal models) to alter CNS gene expression and thereby the intrinsic generation of molecules involved in neural plasticity and neural regeneration, and thereby modifying ultimately behaviour.<ref>{{cite journal | vauthors = Thome J, Hässler F, Zachariou V | title = Gene therapy for psychiatric disorders | journal = The World Journal of Biological Psychiatry | volume = 12 | issue = Suppl 1 | pages = 16–18 | date = September 2011 | pmid = 21905989 | pmc = 3394098 | doi = 10.3109/15622975.2011.601927 }}</ref>

In recent years, it was possible to modify ethanol intake in animal models. Specifically, this was done by targeting the expression of the aldehyde dehydrogenase gene (ALDH2), lead to a significantly altered alcohol-drinking behaviour.<ref>{{cite journal | vauthors = Ocaranza P, Quintanilla ME, Tampier L, Karahanian E, Sapag A, Israel Y | title = Gene therapy reduces ethanol intake in an animal model of alcohol dependence | journal = Alcoholism: Clinical and Experimental Research | volume = 32 | issue = 1 | pages = 52–57 | date = January 2008 | pmid = 18070247 | doi = 10.1111/j.1530-0277.2007.00553.x | hdl-access = free | hdl = 10533/139024 }}</ref> Reduction of p11, a serotonin receptor binding protein, in the nucleus accumbens led to depression-like behaviour in rodents, while restoration of the p11 gene expression in this anatomical area reversed this behaviour.<ref name="Reversal of depressed behaviors in"/>

Recently, it was also shown that the gene transfer of CBP (CREB (c-AMP response element binding protein) binding protein) improves cognitive deficits in an animal model of Alzheimer's dementia via increasing the expression of BDNF (brain-derived neurotrophic factor).<ref>{{cite journal | vauthors = Caccamo A, Majumder S, Richardson A, Strong R, Oddo S | title = Molecular interplay between mammalian target of rapamycin (mTOR), amyloid-beta, and Tau: effects on cognitive impairments | journal = The Journal of Biological Chemistry | volume = 285 | issue = 17 | pages = 13107–20 | date = April 2010 | pmid = 20178983 | pmc = 2857107 | doi = 10.1074/jbc.M110.100420 | doi-access = free }}</ref> The same authors were also able to show in this study that accumulation of amyloid-β (Aβ) interfered with CREB activity which is physiologically involved in memory formation.

In another study, it was shown that Aβ deposition and plaque formation can be reduced by sustained expression of the neprilysin (an endopeptidase) gene which also led to improvements on the behavioural (i.e. cognitive) level.<ref>{{cite journal | vauthors = Spencer B, Marr RA, Rockenstein E, Crews L, Adame A, Potkar R, Patrick C, Gage FH, Verma IM, Masliah E | display-authors = 6 | title = Long-term neprilysin gene transfer is associated with reduced levels of intracellular Abeta and behavioral improvement in APP transgenic mice | journal = BMC Neuroscience | volume = 9 | pages = 109 | date = November 2008 | pmid = 19014502 | pmc = 2596170 | doi = 10.1186/1471-2202-9-109 | doi-access = free }}</ref>

Similarly, the intracerebral gene transfer of ECE (endothelin-converting enzyme) via a virus vector stereotactically injected in the right anterior cortex and hippocampus, has also shown to reduce Aβ deposits in a transgenic mouse model of Alzeimer's dementia.<ref>{{cite journal | vauthors = Carty NC, Nash K, Lee D, Mercer M, Gottschall PE, Meyers C, Muzyczka N, Gordon MN, Morgan D | display-authors = 6 | title = Adeno-associated viral (AAV) serotype 5 vector mediated gene delivery of endothelin-converting enzyme reduces Abeta deposits in APP + PS1 transgenic mice | journal = Molecular Therapy | volume = 16 | issue = 9 | pages = 1580–6 | date = September 2008 | pmid = 18665160 | pmc = 2706523 | doi = 10.1038/mt.2008.148 | id = {{ProQuest|1792610385}} }}</ref>

There is also research going on on [[genoeconomics]], a [[protoscience]] that is based on the idea that a person's [[financial]] behavior could be traced to their [[DNA]] and that [[genes]] are related to [[economic behavior]]. {{as of|2015}}, the results have been inconclusive. Some minor correlations have been identified.<ref>{{cite news| vauthors = Neyfakh L |title=In search of the money gene|url=http://www.boston.com/bostonglobe/ideas/articles/2012/05/13/webhed_are_we_born_to_be_poor_the_rise_of_genoeconomics/?page=full|work=The Boston Globe|date=May 13, 2012}}</ref><ref>{{cite news | vauthors = Entine J |title=Genoeconomics: Is Our Financial Future In Our Chromosomes? |url=https://www.science20.com/jon_entine_contrarian/genoeconomics_our_financial_future_our_chromosomes-95173 |work=Science 2.0 |date=14 October 2012 }}</ref>

Some studies show that our genes may affect some of our behaviors. For example, some genes may follow our state of stagnation, while others may be responsible for our bad habits. To give an example, the MAOA (Mono oxidase A) gene, the feature of this gene affects the release of hormones such as serotonin, epinephrine and dopamine and suppresses them. It prevents us from reacting in some situations and from stopping and making quick decisions in other situations, which can cause us to make wrong decisions in possible bad situations. As a result of some research, mood states such as aggression, feelings of compassion and irritability can be observed in people carrying this gene. Additionally, as a result of research conducted on people carrying the MAOA gene, this gene can be passed on genetically from parents, and mutations can also develop due to later epigenetic reasons. If we talk about epigenetic reasons, children of families growing up in bad environments begin to implement whatever they see from their parents. For this reason, those children begin to exhibit bad habits or behaviors such as irritability and aggression in the future.<ref name="pmid8211186">{{cite journal | vauthors = Brunner HG, Nelen M, Breakefield XO, Ropers HH, van Oost BA | title = Abnormal behavior associated with a point mutation in the structural gene for monoamine oxidase A | journal = Science | volume = 262 | issue = 5133 | pages = 578–580 | date = October 1993 | pmid = 8211186 | doi = 10.1126/science.8211186 | bibcode = 1993Sci...262..578B }}</ref>