This is unexpected again,although hindsight tells us that the pattern is certainly prospective ofgenetic oddity.
This does not apply todepression caused by physical exhaustion which is the common form and thatincludes emotional exhaustion which surely disturbs the metabolism in the sameway as physical exhaustion.
I suspect the genetictriggered depression also has a similar metabolic pathway.
In the event, realdepression is a dangerous malady and a sufferer often needs medicaltreatment, I suspect all forms ofdepression can generate the maximum symptoms and those are surprising the firsttime encountered. I had one suchencounter in my life when young and that was scary enough to ensure tightpersonal control over any driving circumstances. When a person realizes that your own mind andbiochemistry can play you it is not too hard to impose discipline that preventsit.
Unfortunately many look tochemical solutions. Getting annoyed is abetter solution as well as simply engaging in social activity to distract themind. Yet it is hard to query your ownresponses to stimuli objectively and more so to learn how to do so.
Just as you must ask whyyou are suddenly angry, when in another circumstance no such thing would haveoccurred, you must ask why you are unhappy. The reality is that we are hugely affected by blood sugar balances inparticular and that is controlled by sleep and cumulative wok and cumulativeemotional stress.
It would be wonderfullybeneficial if we could devise a monitoring device on our cell phone thattracked our biochemistry and informed us when we increasingly vulnerable and totake evasive action. It may well bepossible and it may be readily applied to others on demand. I think this is one toy our civilizationactually could use.
Released: 11/30/2010 5:20 PM EST
--Finding by CHOP Researchers Points to Disruptions in Brain SignalingNetworks--
Newswise — A largegenetic study of people with major depression has found that a duplicatedregion of DNA on chromosome 5 predisposes people to the disorder. The geneinvolved plays an important role in the development of nerve cells, adding toevidence that disruptions in neurotransmission networks form a biological basisfor depression.
“The copy numbervariations we discovered were exclusive to people with depression, and werelocated in a gene region important in signaling among brain cells,” said studyleader Hakon Hakonarson, M.D., Ph.D., director of the Center for AppliedGenomics at The Children’s Hospital of Philadelphia. “This finding extends workby other researchers suggesting that disruptions in neurotransmitter networksin the brain are an underlying cause of major depressive disorders.”
The study appearsonline today in Public Library of Science One (PLoS One).
The current research isthe first large-scale genome-wide study of copy number variation (CNV) in majordepressive disorder (MDD), a major psychiatric and behavioral disorderaffecting an estimated 16 percent of the U.S.
Hakonarson’s groupconducted a whole-genome scan of DNA from 1,693 patients with MDD, mainly froma European database, and from 4,506 control subjects.
The researchersidentified 12 CNVs exclusive to MDD cases. Their most notable finding was alarge duplication of DNA segments on chromosome 5q35.1, a CNV shared by fiveunrelated patients and not observed in healthy controls. Residing at thatlocation is the gene SLIT3, which is involved in axon development. The axon isthe portion of a neuron that carries nerve impulses away from the cell body.
Hakonarson added thathe plans follow-up studies with more refined sequencing technology, in which heexpects to identify many more CNVs and possibly other types of mutations in theSLIT3 gene, as well as in other functionally related genes that may predisposeto depression. Further studies may also reveal how strongly CNVs at SLIT3 andother related genes contribute to the risk of depression.
“Clinical applicationsfor our discoveries are still in the future, but it may be possible at somepoint to incorporate these findings into personalized medicine,” Hakonarsonsaid. “Identifying causative genes may suggest future targets for drugdevelopment, and may also help us predict a person’s future risk of developingdepression,” he added.
Hakonarson’s group usedgenotype data from the Genetic Association Information Network and from thedatabase of Genotype and Phenotype (dbGaP) of the National Institutes of Health.Funding for the study came from an Institutional Development Award from TheChildren’s Hospital of Philadelphia and from a Research Development Award fromthe Cotswold Foundation.
“Duplication of the SLIT3 Locus on 5q35.1 Predisposes to Major DepressiveDisorder,” PLoS One,published online Dec. 1, 2010.
“Duplication of the SLIT3 Locus on 5q35.1 Predisposes to Major DepressiveDisorder,” PLoS One,published online Dec. 1, 2010.
About The Children’s Hospital of Philadelphia :The Children's Hospital of Philadelphia
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