There have been another two intriguing studies related to autism which adds further to the mystery of the disorder. One study confirms earlier studies which described changes in the nerve cell or neuron structure in autism which do not occur with most other disorders associated with mental retardation. Another study somewhat contradicts previous studies in a disorder associated with autism.
In order to understand some of the terms in this article some basic details are explained.
There are several parts of neurons or nerve cells. These are
1. The synapses.
2. The dendrites.
3. The cell body.
4. The axon.
There are about 100 billion nerve cells in the brain.
Dendrites are fibres which receive information from other neurons. The dendrites are tree-shaped. Dendron means “tree” in Ancient Greek. Dendrites have protruberances on their surface called dendritic spines rather like leaves on a tree. Dendritic spines/leaves have receptors or synapses on their surface. Synapse means “connection” in Ancient Greek. Synapses receive chemicals or neurotransmitters from other nerve cells. The axon is a single fibre which transmits information to other neurons. Axon means “to go or to travel” in Ancient Greek.
Generally speaking diseases which are associated with mental retardation are associated with reduced numbers and density of dendritic spines/leaves on the dendrites of neurons.
The degree of dendritic spine/leaf loss/abnormalities appears to be related to the age of the patient and severity of mental retardation. In mental retardation the short thick spines/leaves are reduced, but long thin spines/leaves are increased in number in the surface of the brain (cortex). This is described in the summary of “Dendritic Spine “Dysgenesis” and Mental Retardation” by Dominick P. Purpura from 1974
However, in 2005: the Neuropathology of Autism, A Review by Jane Pickett, PhD and Eric London, MD confirmed that “contrary to the usual association of spine loss with mental retardation, increased spine density was most pronounced in the lowest functioning subgroup of cases, whereas autism spectrum disorder subjects with either mild or no mental retardation were similar to controls.”
i.e. the opposite of spine/leaf density in other disorders associated with mental retardation.
This latest study titled “Increased dendritic spine densities on cortical projection neurons in autism spectrum disorders” by Hutsler J.J. and Zhang H. in November 2009 confirms that increased spine densities were most commonly found in autism spectrum disorder subjects with more severe mental retardation.
Another condition called Fragile X syndrome is also associated with the clinical features of autism and increased dendritic spine density. However, in Fragile X syndrome even though spine density is increased it is the immature and long spines which are increased in number. The synapses on the long, thin spines are immature. This may be in keeping with Professor John Armstrong`s research that suggests that synapse development depends on normal spine development.
In a recent study of Fragile X syndrome from October 2009 Carlos Portera-Cailliau, assistant professor of neurology and neurobiology at the University of California noted that there was no increase in the density of immature long spines but the turnover of the dendrites was increased.
As with autism there is an association between Fragile X syndrome and an activated immune system.
In summary, shorter and fewer dendritic spines/leaves tend to be the norm for disorders associated with mental retardation and psychiatric disease in the so-called “tree-model” of brain disorders. However, in autism and Fragile X syndrome the spines/leaves have been reported to be increased in density in the past.
The spines/leaves in Fragile X syndrome in this latest study are not increased but dendrite turnover is increased. The spines/leaves in autism are confirmed to be increased in number in the other recent study. The abstract does not mention if the increased spines/leaves are long, thin and immature or mature.
It is possible that perhaps dendrites and/or their spines/leaves are not surviving as long as normal in autism and Fragile X syndrome due to an inflammatory process i.e. “dendritis” and do not have the chance to mature. Long, thin dendritic spines may have fewer mature synapses which may lead to reduced electrical firing rates and the clinical features of autism. It would be interesting to know the dendritic spine/leaf turnover time in autism.
Once again autism is posing more questions than answers.