Cognitive‐behavioural family interventions for schizophrenia have demonstrated utility in reducing relapse rates and improving functional status, but there is little information on the routine application of this work. In the current study therapists in standard health care settings were trained in delivering a cognitive‐behavioural intervention to clients and families. Six months to 3 years after the family training, 45 therapists reported the number of families they had systematically treated, and the difficulties they had encountered. Sixty‐nine per cent reported giving three sessions or more of the intervention to at least one family, but only 18% had used it with three or more families. Therapists reported particular difficulty integrating the family work with their other responsibilities and interests: Allowance of time to undertake the intervention, afterhours scheduling, and illness or holidays presented particular difficulties. Only 4% reported that their knowledge of behavioural techniques was a significant problem, but in a written test most therapists did not display minimum recall of the material on cognitive therapy, social skills training, or behavioural strategies. Therapists also reported whether they had used segments of the intervention in their routine clinical contacts. Over 80% said they applied all segments of the intervention at least once a month, but the frequencies for cognitive and behavioural strategies fell below 40% when they were corrected for recall of the segments. This study demonstrated significant problems in disseminating cognitive‐behavioural approaches to multidisciplinary settings.
The Anterior Cingulate Cortex (ACC, Brodmans Area 24) is implicated in the pathogenesis of schizophrenia due to its normal functions and connectivity together with reports of structural, morphological and neurotransmitter aberrations within this brain area in the disease state. Two-dimensional gel electrophoresis (2DE) was employed to scan and compare the ACC gray matter proteomes between schizophrenia (n = 10) and control (n = 10) post-mortem human tissue. This proteomic approach has detected 42 protein spots with altered levels in the schizophrenia cohort, which to our knowledge is the first proteomic analysis of the ACC in schizophrenia. Thirty nine of these proteins were subsequently identified using mass spectrometry and functionally classified into metabolism and oxidative stress, cytoskeletal, synaptic, signalling, trafficking and glial-specific groups. Some of the identified proteins have previously been implicated in the disease pathogenesis and some offer new insights into schizophrenia. Investigating these proteins, the genes encoding these proteins, their functions and interactions may shed light on the molecular mechanisms underlying the heterogeneous symptoms characteristic of schizophrenia.
Alterations in the circuitry between and within different brain regions including the anterior cingulate cortex (ACC) is implicated in the neuropathology of schizophrenia. The involvement of white matter in schizophrenia is becoming increasingly apparent with reports of structural, morphological and genetic alterations occurring in the disease. The 2-DE was employed to reveal significantly altered proteins within the ACC white matter proteome in a schizophrenia cohort (n = 10) relative to controls (n = 10). From the 423 matched spots between the two groups, the levels of 32 protein spots were altered in the schizophrenia ACC white matter. Of these, 30 spots were identified using MS. The majority of the altered proteins in schizophrenia function in metabolism, the cytoskeleton, and the synapse. These proteomic data suggest that the brain circuitry involving the ACC white matter tracts is altered in schizophrenia, possibly caused by depleted glucose metabolism and altered structural components of this region.
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