Lack of selection in ASPM gene haplotype

Comment on “Ongoing Adaptive Evolution of ASPM, a Brain Size Determinant in Homo sapiens” — Yu et al. 316 (5823): 370b — Science

Some new evidence contradicting previous claims that a particular haplotype of the ASPM gene was selected. We posted about some related work in 2005.

An excerpt:

We also assessed evidence for selection at ASPM by carrying out the long-range haplotype (LRH) test (9). This test assesses whether a haplotype is too young to have risen to its frequency without selection. The LRH test is not affected by uncertainty in recombination rate estimates. We compared LRH results for the A44871G polymorphism to SNPs of matched frequency in HapMap CEU (3, 10) (Fig. 1C). We observed at least as strong a signal for selection at 90% of the regions examined (3, 11). Several genome-wide surveys using similar methods also failed to find evidence for selection at ASPM in European-derived populations (4, 12, 13). The one survey that did find a signal near ASPM did so only in individuals of Chinese ancestry (13), failing to support the contention of (1) of recent selection in European history. Based on linkage disequilibrium (LD) breaking down within ~100 kb on either side (Fig. 1B), we estimate that the G allele arose in European history at least tens of thousands of years ago and possibly more than 100,000 years ago (14) (table S3 and SOM Text). These dates are difficult to reconcile with selection ~6000 years ago, as suggested in (1).

Cognitive dysfunction in young subjects who have a gene for frontotemporal dementia

This isn’t news but is rather an interesting thing I learned today. There is a family with an inherited form of frontotemporal dementia. In this family, the onset of dementia occurred between 57-63 years of age. A study was done which did psychological tests on members of this family. It was found that young people (younger than 35) who carried the gene for the disorder had measurable frontal-executive dysfunction (whereas controls, young people in the same family who did not carry the gene, did not have dysfunction).

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Enabling Neural Engineering Ought To Be The Measure Of Neuroscience

The field of neuroscience naturally focuses its inquiry into neurons. This approach to understanding the brain by studying its parts has been thought to have a greater potential than that of psychology to understand how the brain works, a comment made by no less than Daniel L. Schacter, chair of Harvard’s Department of Psychology, in his book, The Seven Sins of Memory.

However promising the field has been thus far, even the most accomplished neuroscientists will admit that we still do not understand how the brain really works. I would submit that the current reductionist nature of neuroscience has shed much light on the dynamics of how neurons work, but has to a far lesser degree shed light on how neurons process information. The difference between these two lines of inquiry is important for making progress in understanding how the brain works.
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More halorhodopsin

This week’s Nature has quite a few additional halorhodopsin articles for photochannel fans.

Halorhodopsin article from Deisseroth’s lab:
Multimodal fast optical interrogation of neural circuitry [News & Views]

Also, there is an intriguing article on both the general excitement in the neuroscience community with this new technology and a possible intellectual property dispute over it.

Interview on USC hippocampal prosthesis

Interview with Ted Berger of USC on their hippocampal prosthetic project in Popular Science magazine

To summarize the most interesting info from the interview:

Berger’s team is trying to make a hippocampal prosthesis (a chip that could be implanted in the hippocampus and help people with damaged hippocampuses). (we’ve mentioned Berger’s team’s efforts before).

He admits that he doesn’t understand how the hippocampus functions in memory, but argues that you may be able to make a prosthesis without this understanding: “A repairman doesn’t need to understand music to fix your broken CD player.”

The first crucial test will be done later this year by Sam Deadwyler at Wake Forest. He will implant the chips in rats, deactivate their hippocampuses with drugs, and see if the prosthetic helps.