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Posts Tagged ‘obsessive-compulsive’

rs25532

“I know it now … that I am here to love her. I love her I love her I love her and she doesn’t even have to tell me she loves me back. That’s how much I love her.”

“There there. Just breathe. I wish you would stop obsessing about everything. This week it is Selena Gomez and last week it was Leela from Futurama. You really need to integrate your everyday thoughts and feelings separately from your fantasy life otherwise people are going to ostracize you.”

“I love ostriches so much.”

“Listen. Stop browsing 23andMe data. Just because the “C” allele at rs25532 increases the transcriptional efficiency of the serotonin transporter does not mean that being an LPR “long/long”, rs25532 “C/C” gives you a license to act obsessively. I mean, you’re a TIGER! You don’t even have those alleles.”

“She’s just so beautiful. I want to scratch your eyes out.”

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Kim Kardashian
Image by BiggerPictureImages.com via Flickr

Sometimes, when flipping channels late at night, its hard NOT to stop and gawk at the various spectacles on reality-trash-TV.  No self-respecting scientist would admit to being smitten by all the vanity and preening – right?  Well, back in 2002, there was a mouse whose homeobox-B8 gene was disrupted – who caused a minor media sensation in the community – for its tendency toward, “excessive grooming … not unlike that of humans suffering from the OC-spectrum disorder”.  Hunh?  A mouse not-unlike trash-TV celebs who can’t stop fixing their hair?  An interesting genetic effect to be sure.

A recent paper, “Loss of Hoxb8 alters spinal dorsal laminae and sensory responses in mice” reports a closer look at this mouse mutation and provides evidence that the excessive grooming is, instead, a consequence merely of “itch perception” which arises from disrupted development of itch specific GrpR-positive neurons in lamina I of the dorsal spinal cord“.  Indeed, when the investigators applied sub cutaneous lidocaine to the peripheral nerve endings in the groomed regions – the excessive grooming stopped.  If you are interested in the development of the peripheral nervous system, the paper is well worth a read!  If you are into the psychology of excessive grooming, the Kardashian sisters always provide a steady stream of data.

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silver copy of a 1930 penny
Image via Wikipedia

In their forecast “The World in 2010” special issue, the Economist points to “The looming crisis in human genetics” wherein scientists will reluctantly acknowledge that, even with super-cheap genome sequencing tools, we may not soon understand how genetic variation contributes to complex illness.  The argument is a valid one to be sure, but only time will tell.

A paper I read recently, reminded me of the long hard slog ahead in the area of genomics and psychiatric illness.  The authors in “Association of the Glutamate Transporter Gene SLC1A1 With Atypical Antipsychotics–Induced Obsessive-compulsive Symptoms” [Kwon et al., (2009) Arch Gen Psychiatry 66(11)] are trying to do something very important.  They would like to understand why certain (most) psychiatric medications have adverse side-effects and how to steer patients clear of adverse side-effects.  This is because, nowadays, a patient learns via a drawn-out trial-and-error ordeal about which medications he/she can manage the benefits/costs.

Specifically, the authors focused their efforts on so-called obsessive-compulsive symptoms that can arise from treatment with atypical antipsychotic medications.  Working from 3 major medical centers (Samsung Medical Center, Seoul National University Hospital and Asan Medical Center) Kwon et al., were able to cobble together a mere 40 patients who display these particular adverse side-effects and matched them with 54 patients based on several demographic and medication-based criteria.  Keep in mind that most genetic studies use upwards of 1,000 samples and still – hardly – are able to obtain significant effects.

Nevertheless, the authors note that the glutamate transporter gene (SLC1A1 or EAAC1) is a most logical candidate gene, being a located in a region mapped for obsessive-compulsive disorder risk and also a gene that appears to be down-regulated in response to atypical anti-psychotic treatment (particularly clozapine).  A series of statistical association tests for 10 SNPs in this gene reveal that two SNPs (rs2228622 and rs3780412) and a 3-SNP haplotype (the A/C/G haplotype at rs2228622-rs3780413-rs3780412) showed modestly significant association (about 4-fold higher risk) with the adverse symptoms.

To me, this is a very noteworthy finding.  A lot of work went into a very important problem – perhaps THE most pressing problem for patients on anti-psychotic medications today – and the results, while only of modest significance, are probably biologically valid.  The authors point out that rs2228622 and rs3780412 have previously been associated with OCD in other studies.

But when you compare these modest results (that these authors fought hard to obtain) with the big promises of the genomic era (as noted in the Economist article), well then, the results seem rather diminutive.  Will all patients who carry the risk haplotype be steered away from atypical antipsychotics?  Will big pharma (the authors of this paper disclose a great many ties to big pharma) support the fragmentation of their blockbuster drug markets into a hundred sub-populations?  I doubt it.  But some doctors and patients will experiment and continue to explore this avenue of inquiry – and it will take a long time to work out.  Better check back in 2020.

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