Wednesday, 9 November 2011

Brains, epigenetics and neuron numbers

In a post a few months back on 'what do we know about autism' I discussed some of the various views and opinions that certain professionals have about autism spectrum conditions. Although not exactly a complete picture of such a heterogeneous condition like autism, summarising what we know (and don't know) about 'general autism' at least provides a starting point for where research might want to 'project' itself in future.

In among the various findings, research on the brain and autism figured heavily; highlighting the issue of head size and brain growth alongside the fact that autism is not, generally speaking, due to a localised brain issue. With this in mind, a few interesting studies have been published in recent days which require some comment.

The first study by probably one of the most well-known names in autism brain research, Eric Courchesne and colleagues* suggested that in one part of the brain, the prefrontal cortex, children with autism might have more brain cells (neurons) than control children.  Based on examination of post-mortem prefrontal brain tissue, the numbers of neurons were counted from 7 children with autism and compared with 6 controls. The results suggested that the total numbers of neurons were increased in the autism group, and specifically in the dorsolateral prefrontal cortex. This alongside findings of a heavier brain in autism compared to controls.

Bearing in mind the small participant numbers and the fact the neurons can only really be counted when someone is deceased, there is some interest in this paper. The prefrontal cortex (I am reliably informed) is linked to quite a few things including social and communicative behaviours; areas with more than a passing relationship to autism. I would hasten to add that there are lots of other correlated functions and behaviours to this area as there is with other brain areas. You might think, more neurons = better functioning in these areas but unfortunately things are not so straight-forward, hence the reason why we tend prune our brain cells during certain points of our lives. Efficiency it seems trumps quantity.

The second paper, by Shulha and colleagues** also looked at brains and indeed the same region of the brain as Courchesne and colleagues, the prefrontal cortex, looking to characterise the epigenetic signature of autism. Epigenetics is basically environment; changes to gene activity not down to changes in DNA. Looking at post-mortem brain tissue from 16 people with autism and 16 controls, they examined samples for a specific epigenetic signature, histone methylation, and found many, many loci affected by altered histone methylation, most of which were not down to DNA mutation. In most cases, genes were switched on or off for reasons other than mutation (SNPs).

In both these papers, there is an interesting intersection between brain, genes and environment. The prefrontal cortex is one of the majority of brain areas that develop early on in-utero hence speculation has turned to some prenatal factor as potentially being involved. My mind wanders back to the study on vits and SNPs at this point, as one of a number of potentially interesting correlations. I do wonder if we ought also to be looking back at some older research on a possible role for disordered endogenous opioid peptide chemistry as potentially being involved in their role as neuronal pruning agents. Without trying to sound too 'he does not know what he is talking about' how about any involvement from the caspases also?

* Courchesne E. et al. Neuron number and size in prefrontal cortex of children with autism. JAMA. Novemeber 2011.
** Shulha HP. et al. Epigenetic signatures of autism. Archives of General Psychiatry. November 2011.

1 comment:

  1. The methods of the linked study said it was looking at kids ages 7.55-13. 4years with an average age of 10.20

    Also the IQ of the participants in the linked study was 101 + /-16 (indicating about average IQ for the participants in the asd participants). This implies it didn't included the more severely impacted of our kiddos who make up a significant portion of the population.

    These are huge confounds compaired to eric's sleep MRI study that looked at infants.


    By age 7 we are past a lot of the important sensitivity periods, early intervention treatments (for those able to access them), and have had significant maturation processes.

    I would have to say this particular study is not a viable candidate for comparison to Eric's or discussion on DIAGNOSIS as trained diagnostians with experience in diagnosing autism can do so at ages 1.5-3 years old depending on severity of impact. The case for wanting to use sleep MRI findings for diagnosing apply to the under 3 population when there are less of those maturation and life experience confounded. In fact Eric mentions the reason they did the sleep MRIs with 1-2 year olds was specifically to avoid that very confound.

    Although the study you are linking remains an interesting read and an important finding about how much brain change is possible by 7.55-13. 4 years old.

    ReplyDelete