New Study: Adverse childhood experiences influence white matter microstructure in patients with schizophrenia


The association of adverse childhood experiences to reduced fractional anisotropy and increased mean diffusivity in key White Matter tracts contributing to the functional integrity of the brain suggests that adverse childhood experiences might contribute to the pathophysiology of schizophrenia through a detrimental action on structural connectivity in critical cortico-limbic networks [of the brain].


Any severe detriment to the function of the corpus callosum that connects the two brain hemispheres can have a tremendous impact upon those who have difficulties with accurate perception and processing of sensory stimulations. Accurate appraisal and functional response to environmental challenges are highly dependent upon effective connectivity between the more “perceptive” and “sensory” right… and the more “learned” and “judicious” left hemispheres. If they get out of whack with each other, look out.

The big names here are Antonio Damasio, Michael Gazzaniga, Louis Cozolino, Joseph Ledoux, Jak Pansepp, and Iain McGilchrist.

@SoitGoes (I think it was, but I might be wrong) posted this study information the other days which is related to this topic and that is also interesting, tying in the Glutamate hypothesis into this:

In an accompanying commentary, Bita Moghaddam, PhD, professor of neuroscience and of psychiatry, University of Pittsburgh, suggests that if excess glutamate is driving schizophrenia in high-risk individuals, it may also explain why a patient’s first psychotic episodes are often caused by periods of stress, since stress increases glutamate levels in the brain.


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Given what glutamate does (it’s the brain’s #1 excitatory neuroxmitter by far), a growing heap of research has been pointing at glutamate problems underlying sz and other psychotic disorders – especially highly positive-symptom sz, bipolar, rapid cycling / cyclothymia, etc. – for about a decade and a half, I think.

Wasn’t glutamante hypothesis discarded when Eli Lilly tried LY2140023?

Not at all - their drug candidate just didn’t work - lots of dopamine targeted medication candidates also don’t work.

The glutamate hypothesis is just an add-on to the dopamine theory - they are most likely both accurate - and vary by person in terms of the impact on a given person.