Moore et al

With an “adolescent onset”, schizophrenia, without a doubt, is a neurodevelopmental disorder. Even though very rare, cases with 13 years old children have been evident. Moore et al does an impeccable job creating similar morphological differences in the brain that has been shown in patients with schizophrenia while using a rat model. 

By administering methylazoxymethanol acetate (MAM), a DNA-alkylating agent, on embryonic day 17 (E17), brought forth anatomical abnormalities in rats that are similar to schizophrenia.  MAM E17 rat model makes a great neurodevelopmental model for schizophrenia and has been viewed as the animal model of schizophrenia in the science community. Unlike previous research papers we have read, this paper looks at the Neuroanatomy rather than using behavioral testing. Being one of the major symptoms of patients with schizophrenia, hallucination would have been problematic to see in animals since there is no sufficient evidence regarding animals hallucinating. This comes from the fact that hallucinating related behaviors such as response to non-apparent stimuli, are viewed to be too non-specific for any research that is trying to look at the mechanisms of hallucinations. This makes looking at the dysfunction in genes, neurochemistry and Neuroanatomy in schizophrenia a more promising animal model.

Early administration of MAM in “Figure 4” showed less thickness and area in areas such as the PFC and hippocampus in MAM E15 than MAM 17. This shows the neurodevelopmental problem that causes these brain areas to decrease more in size when MAM is administered earlier. It would have been interesting to look at genetic predeterminants such as DISC-1, which is important when it comes to development. The DNA damage that was caused by MAM can help see which genes are involved in neurodevelopment and whether some of these genes might contribute to neurodegenration. Even though they mentioned how DNA methlyation may regulate the expression of certain genes, it would have been nice if they went along with it and put their ideas in action.

Also, in “Figure 7”, where they were measuring for ataxia, was not the best choice when it comes to looking at the neuropathology of schizophrenia. This is because MAM causes lack of muscle control and there is no association between ataxia and schizophrenia that I know of. There might have been a reason behind them choosing to go through with this particular experiment that I have overlooked. If this was a study on epilepsy, it could have been beneficial to measure the levels of ataxia.