Brain dysfunction schizophrenia

S100B Developmental brain dysfunction, learning and memory deficits Alzheimer s disease, blood brain barrier dysfunction Down syndromebrain trauma and ischemia, schizophrenia, depression... 

Mounting radiological evidence from PET, MRI, and CT scans confirms the presence of chronic brain dysfunction (PET scans) and brain atrophy (MRI and CT scans) in neuroleptic-treated patients diagnosed with schizophrenia. It also confirms the brain-disabling concept. 

Brunet-Gouet E, Decety J. 2006. Social brain dysfunctions in schizophrenia A review of neuroimaging studies. Psychiatry Res 148 75-92. 

Prabakaran, S., Swatton, J. E.,Ryan, M.M. etal. Mitochondrial dysfunction in schizophrenia evidence for compromised brain metabolism and oxidative stress. Mol. Psychiatry, 9 684-697, 2004. 

Lewis, D. A. (2000) GABAergic local circuit neurons and prefrontal cortical dysfunction in schizophrenia. Brain Res. Rev. 31,270-276. 

Traditionally, most affective disorders have been treated with compounds that resemble the neurotransmitters that are deficient or in excess in specific brain regions. The aberrant levels of neurotransmitters (or their receptors), such as norepinephrine, dopamine, acetylcholine, and serotonin, have correlated with behavioral symptoms of schizophrenia, depression, anxiety, sleep disorders, motor dysfunctions, attention difficulties, and cognitive disorders. Most drugs discovered for these disorders resulted from screening compounds directly in rodent behavioral models that mimic the behavior of the disease. In these cases, the molecular target" or mechanism of action was assumed to be the deficiency or excess of a neurotransmitter. 

The neurochemistry of schizophrenia has been considered in a variety of ways by numerous investigators and most have, as here, focussed on the role of abnormalities and/or dysfunction of brain neurotransmitter systems in the disease. Implicit in a book on the neurochemistry of consciousness is the assumption that this chapter will address the neurochemical basis of the disturbance (s) of consciousness that occurs in schizophrenia. Consciousness in its particular and generally-understood meaning is not obviously distorted in schizophrenia, although schizophrenic patients clearly have a different, or abnormal experience of the external world—their conscious awareness is disturbed. 

We also see increasing use for P MRS in studying mental illnesses. The ability to characterize tissue energetics (via PCr and ATP) and phospholipid metabolism (via PMEs and PDEs) in sufficiently localized brain regions should help clarify the roles of mitochondrial dysfunction and phospholipid metabolism in schizophrenia and BD, as suggested by earlier efforts... 

The co-3 fatty acids have numerous important functions, especially in the brain. Accordingly, a deficiency of DHA and EPA may cause dysfunction of the central nervous system and probably also the retina, thereby resulting in impaired vision. In addition, there is a variety of neurological and psychiatric disorders that have been associated with decreased levels of especially DHA and AA, such as, for example, schizophrenia and depression [3], post-traumatic stress syndrome, autism and attention deficit hyperactivity disorder. Since no primary inherited defect of essential fatty acid interconversion has yet been described, no specific explanations for the essential fatty acid concentration changes are readily available. 

If schizophrenia is caused by abnormal early brain development (cf. Figs. 10—15 and 10—16), it may be virtually impossible to reverse such abnormalities in adulthood. On the other hand, some day it may be possible to compensate for such postulated neurodevelopmental difficulties by other mechanisms or to interrupt an ongoing mechanism still present in the symptomatic patient. Therefore, it will be critical to learn what neurodevelopmental abnormalities may exist in schizophrenia in order to devise strategies for reducing their potential impact. It may even be possible to identify such abnormalities in presymptomatic individuals or to exploit the plasticity of adult neurons to compensate for neurodevelopmentally endowed dysfunction. These are bold and unsubstantiated theoretical extrapolations based on... 

Alan Mackay-Sim, Francois Feron, Darryl Eyles, Thomas Bume, and John McGrath Possible Contributions of Myelin and Oligodendrocyte Dysfunction to Schizophrenia Daniel G. Stewart and Kenneth L. Davis Brain-Derived Neurotrophic Factor and the Plasticity of the Mesolimbic Dopamine Pathway Oliver Guillin, Nathalie Griffon, Jorge Diaz,... 

Waddington, J. L., O Callaghan, E., Larkin, C., Kinsella, A. 1993, Cognitive dysfunction in schizophrenia organic vulnerability factor or state marker for tardive dyskinesia , Brain Cogn., vol. 23, no. 1, pp. 56-70. 

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