Despite a lack of recent progress in the treatment of schizophrenia, our understanding of its genetic and environmental causes has considerably improved, and their relationship to aberrant patterns of neurodevelopment has become clearer. This raises the possibility that 'disease-modifying' strategies could alter the course to — and of — this debilitating disorder, rather than simply alleviating symptoms. A promising window for course-altering intervention is around the time of the first episode of psychosis, especially in young people at risk of transition to schizophrenia. Indeed, studies performed in both individuals at risk of developing schizophrenia and rodent models for schizophrenia suggest that pre-diagnostic pharmacotherapy and psychosocial or cognitive-behavioural interventions can delay or moderate the emergence of psychosis. Of particular interest are 'hybrid' strategies that both relieve presenting symptoms and reduce the risk of transition to schizophrenia or another psychiatric disorder. This Review aims to provide a broad-based consideration of the challenges and opportunities inherent in efforts to alter the course of schizophrenia.

/pdf/altering-the-course-of-schizophrenia-progress-and-3ar2t81hy7.pdf

Altering the course of schizophrenia: progress and perspectives

The poly(I:C)-induced maternal immune activation model in preclinical neuropsychiatric drug discovery.

Brain changes in a maternal immune activation model of neurodevelopmental brain disorders.

There is extensive bi-directional communication between the brain and the immune system in both health and disease. In recent years, the role of an altered immune system in the etiology of major psychiatric disorders has become more apparent. Studies have demonstrated that some patients with major psychiatric disorders exhibit characteristic signs of immune dysregulation and that this may be a common pathophysiological mechanism that underlies the development and progression of these disorders. Furthermore, many psychiatric disorders are also often accompanied by chronic medical conditions related to immune dysfunction such as autoimmune diseases, diabetes and atherosclerosis. One of the major psychiatric disorders that has been associated with an altered immune system is schizophrenia, with approximately one third of patients with this disorder showing immunological abnormalities such as an altered cytokine profile in serum and cerebrospinal fluid. An altered cytokine profile is also found in a proportion of patients with major depressive disorder and is thought to be potentially related to the pathophysiology of this disorder. Emerging evidence suggests that altered immune parameters may also be implicated in the neurobiological etiology of autism spectrum disorders. Further support for a role of immune dysregulation in the pathophysiology of these psychiatric disorders comes from studies showing the immunomodulating effects of antipsychotics and antidepressants, and the mood altering effects of anti-inflammatory therapies. This review will not attempt to discuss all of the psychiatric disorders that have been associated with an augmented immune system, but will instead focus on several key disorders where dysregulation of this system has been implicated in their pathophysiology including depression, schizophrenia and autism spectrum disorder.

Evidence for a Dysregulated Immune System in the Etiology of Psychiatric Disorders

Aim This study compared the time spent using screen-based media or reading on the functional connectivity of the reading-related brain regions in children aged 8-12. Methods We recruited 19 healthy American children from a private school in Cincinnati, USA, in 2015-6 after advertising the study to parents. The parents completed surveys on how many hours their children spent on independent reading and screen-based media time, including smartphones, tablets, desktop or laptop computers and television. The children underwent magnetic resonance imaging that assessed their resting-state connectivity between the left visual word form area, as the seed area, and other brain regions, with screen time and reading time applied as predictors. Results Time spent reading was positively correlated with higher functional connectivity between the seed area and left-sided language, visual and cognitive control regions. In contrast, screen time was related to lower connectivity between the seed area and regions related to language and cognitive control. Conclusion Screen time and time spent reading showed different effects on functional connectivity between the visual word form area and language, visual and cognitive control regions of the brain. These findings underscore the importance of children reading to support healthy brain development and literacy and limiting screen time.

Brain connectivity in children is increased by the time they spend reading books and decreased by the length of exposure to screen-based media.

The Simple View theory suggests that reading comprehension relies on automatic recognition of words combined with language comprehension. The goal of the current study was to examine the structural and functional connectivity in networks supporting reading comprehension and their relationship with language comprehension within 7-9 year old children using Diffusion Tensor Imaging (DTI) and fMRI during a Sentence Picture Matching task. Fractional Anisotropy (FA) values in the left and right Inferior Longitudinal Fasciculus (ILF) and Superior Longitudinal Fasciculus (SLF), known language-related tracts, were correlated from DTI data with scores from the Woodcock-Johnson III (WJ-III) Passage Comprehension sub-test. Brodmann areas most proximal to white-matter regions with significant correlation to Passage Comprehension scores were chosen as Regions-of-Interest (ROIs) and used as seeds in a functional connectivity analysis using the Sentence Picture Matching task. The correlation between percentile scores for the WJ-III Passage Comprehension subtest and the FA values in the right and left ILF and SLF indicated positive correlation in language-related ROIs, with greater distribution in the right hemisphere, which in turn showed strong connectivity in the fMRI data from the Sentence Picture Matching task. These results support the participation of the right hemisphere in reading comprehension and may provide physiologic support for a distinction between different types of reading comprehension deficits vs difficulties in technical reading.

Right is not always wrong: DTI and fMRI evidence for the reliance of reading comprehension on language-comprehension networks in the right hemisphere

Fluoxetine and aripiprazole treatment following prenatal immune activation exert longstanding effects on rat locomotor response.

In order to identify the contribution of individual serotonin and dopamine receptor subtype binding targets to antipsychotic medication efficacy, we analyzed correlations between binding affinity to cloned dopamine and serotonin receptor subtypes and clinically effective drug dose for atypical antipsychotic medications. The strongest correlation was observed between binding affinity to the D3 subtype dopamine receptor and clinically effective atypical antipsychotic medication drug dose (r = 0.77, p = 0.005). In contrast, binding affinity to the D2 (r = 0.59, p = 0.056) and D4 subtype dopamine receptors (r = 0.23, p = 0.23) exhibited lower correlations with atypical antipsychotic medication dosages. No direct correlations were identified between atypical antipsychotic medication dose and binding affinities to serotonin 5-HT1A, 5-HT2A, 5-HT2C, or 5-HT7 receptor subtypes. Highly significant correlations were also observed between atypical antipsychotic medication dose and the ratios of D2/5-HT1A (r = 0.69, p = 0.019); D3/5-HT1A (r = 0.69, p = 0.02); D3 × 5-HT2A (r = 0.71, p = 0.014); (D2 × D3)/5-HT1A (r = 0.81, p = 0.002); (D2 × D3 × 5-HT7)/5-HT1A (r = 0.74, p = 0.010); (D2 × D3 × 5-HT2A)/5-HT1A (r = 0.76, p = 0.007); (D2 × D3 × 5-HT2C)/5-HT1A (r = 0.76, p = 0.007); and (D2 × D3 × 5-HT2A × 5-HT2C)/5-HT1A (r = 0.72, p = 0.013) receptor binding affinities. These observations suggest opposing interactions among three distinct domains of receptor binding targets contribute to the antipsychotic effects of atypical antipsychotic medications: (1) D3 and D2 dopamine receptor binding affinity enhance atypical antipsychotic medication potency. (2) Binding affinity to serotonin 5-HT2A, 5-HT2C, and 5-HT7 receptors also facilitates antipsychotic efficacy. (3) In contrast, enhanced binding affinity to serotonin 5-HT1A receptor reduces antipsychotic medication potency.

Receptor Binding Targets for Antipsychotic Efficacy

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Right is not always wrong: DTI and fMRI evidence for the reliance of reading comprehension on language-comprehension networks in the right hemisphere

Fluoxetine and aripiprazole treatment following prenatal immune activation exert longstanding effects on rat locomotor response.

Receptor Binding Targets for Antipsychotic Efficacy