New studies show that SAND could be true( i hope).

[aldebaran]

In my theory SAND(Short Axon Nervous Design) I claim that the nerves are wired in a different way in the autistic brain. The nerves in a SAND-brain, will connect at an earlier stage on a given path and therefore not have as many long connections(axons) as in an NT-brain.

This new test shows, as far as I can see, that I am on the right path . If the scientists find after years of advanced studies, that I am right, don't forget to tell them so .

Researchers one step closer to potential autism test

This is a quote from the news article:

Using the MRI, the study authors measured how the water in the brain flows along the axons or nerve fibers in the parts of the brain that control language, social and emotional functioning. The scans revealed that the wiring of the brains of those with autism was disorganized compared with the brains of a typical person without autism. This is how they could determine which brains scans belonged those study participants with autism.

Never underestimate the brain of an autist

Anders

[aldebaran]

I have now send a link to my page about SAND to a member of the team. "JANET E. LAINHART"

If you never try, you don't get anything

[aldebaran]

More information on the nervous system and barin cells saids that connections may be shorter due to short Dendrit.

Interestingly, four rare amino acid coding variants have been identified in the EPAC2 gene in people with autism, suggesting they could help yield insights on the protein’s function. Therefore, the authors overexpressed one of these mutant proteins in cultured rat cortical neurons, and again found reduced basal dendritic complexity and length. This single amino-acid mutation, seen in four people with autism from two families, is located within the Ras association domain of Epac2. The small GTPase Ras has been implicated in neuronal morphogenesis, so this new result suggested that Epac2 may be regulating basal dendritic arbors via its interaction with Ras. The authors tested this by first showing that Epac2 normally interacted with Ras in cultured rat cortical neurons, but that the mutant Epac2 had significantly impaired interactions with Ras. Importantly, disrupting Ras pharmacologically in cultured neurons also reduced basal dendritic complexity and length.

The investigators say future work will involve analyzing the function of Epac2 in vivo, at both the circuit and behavioral level. They add that further studies should also assess the role of Epac2 in human disorders—more rare Epac2 mutations may be found in people with autism, further elucidating its function. It may be that Epac2 is part of a signaling network, as Penzes and his colleagues have previously shown that Epac2 interacts with neuroligins, important autism susceptibility molecules.

Read the rest of the article:
Wiring Up the Newest Part of the Cortex

Regards
A.