Abstract “Internet technology offers psychiatrists new opportunities for remote interaction with patients. It also raises issues regarding therapeutic effectiveness, safety, technical problems and possibilities for overcoming them, and matters related to specific mental health problems such as autism. The case presented concerns an adolescent male with severe social impairment and isolation as manifestations of Asperger’s syndrome.

The patient … accepted contact with psychiatric services through telepsychiatry, which enabled initial assessment and the development of a therapeutic relationship.

In due course the patient was able to attend the clinic in person. He became somewhat reconciled to his family. With appropriate adaptations he was able to resume his education and career.

Telepsychiatry shows promise in engaging with patients with autism spectrum disorders. As experience accrues, there is some evidence that it is safe and effective. Adaptations to traditional clinical psychotherapy may be required.”

Clarke CS: Telepsychiatry in Asperger’s syndrome. Ir. J. Psychol. Med. 35(4): 325-328 (2018).


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Abstract:  “The authors sought to describe the emergent course of bipolar disorder in offspring of affected parents subgrouped by parental response to lithium prophylaxis.

Parent bipolar disorder was confirmed by the best-estimate procedure and lithium response by research protocol. High-risk offspring (N=279) and control subjects (N=87) were blindly assessed, annually on average, with the Kiddie Schedule for Affective Disorders and Schizophrenia-Present and Lifetime version or the Schedule for Affective Disorders and Schizophrenia-Lifetime version. DSM-IV diagnoses were confirmed using the best-estimate procedure in blind consensus reviews. Cumulative incidence and median age at onset were determined for lifetime syndrome- and symptom-level data. Mixed models assessed the association between parent and offspring course. A multistate model was used to estimate the clinical trajectory into bipolar disorder.

The cumulative incidence of bipolar disorder was 24.5%, and the median age at onset was 20.7 years (range, 12.4 to 30.3). The clinical course of the affected parent was associated with that of the affected child. Depressive episodes predominated during the early bipolar course, especially among offspring of lithium responders. Childhood sleep and anxiety disorders significantly predicted 1.6-fold and 1.8-fold increases in risk of mood disorder, respectively, and depressive and manic symptoms predicted 2.7-fold and 2.3-fold increases in risk, respectively. The best-fit model of emerging bipolar disorder was a progressive sequence from nonspecific childhood antecedents to adolescent depression to index manic or hypomanic episode. Subthreshold sleep symptoms were significantly associated with transition from well to non-mood disorder, and psychotic symptoms in mood episodes were significantly associated with transition from unipolar to bipolar disorder.

Bipolar disorder in individuals at familial risk typically unfolds in a progressive clinical sequence. Childhood sleep and anxiety disorders are important predictors, as are clinically significant mood symptoms and psychotic symptoms in depressive episodes.”

Duffy A, Goodday S, Keown-Stoneman C and Grof P: The Emergent Course of Bipolar Disorder: Observations Over Two Decades From the Canadian High-Risk Offspring Cohort. Amer. J. Psychiatry [Epub ahead of print, Dec. 11, 2018; doi: 10.1176/appi.ajp.2018.18040461.].


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Many studies have investigated impairments in cognitive domains in adults with autism spectrum disorder. Yet, to date, a comprehensive overview on the patterns of cognitive functioning is lacking. The present report summarizes the literature on nonsocial and social cognitive functioning in adults with autism spectrum disorder, allowing for comparison of the severity of deficits between different domains.

Results of this systematic review and meta-analysis suggest that adults with autism spectrum disorder show impairments in both social and nonsocial cognitive domains. Specifically, large impairments were found in theory of mind and emotion perception and processing, followed by medium impairments in processing speed and verbal learning and memory. The least altered cognitive domains were attention and vigilance. These findings contribute to the understanding of the patterns of cognitive functioning in these individuals and may assist in the identification of targets for cognitive interventions.

Velikonja T, Fett AK, Velthorst E: Patterns of Nonsocial and Social Cognitive Functioning in Adults With Autism Spectrum Disorder: A Systematic Review and Meta-analysis. JAMA Psychiatry [Epub ahead of print, Jan. 2, 2019; doi: 10.1001/jamapsychiatry.2018.3645.]


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Limits to human neurogenesis – really?

Lucassen PJ, Toni N, Kempermann G, Frisen J, Gage FH, Swaab DF: Limits to human neurogenesis – really? Molecular Psychiatry [Epub ahead of print, January 7, 2019; doi: 10.1038/s41380-018-0337-5.].


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Abstract: “Genetic discoveries about human brain development and neuropsychiatric syndromes have changed the landscape of psychiatric research. The genotyping of hundreds of thousands of individuals has identified many hundreds of genomic regions that are associated with psychiatric diagnoses, and progress is being made in uncovering the specific genes that underlie these statistical associations, although most are still undetermined. While there are great expectations that such genetic discoveries will lead to novel treatments based on fundamental mechanisms of illness, there are important caveats. Individual risk-associated common variants explain only a tiny fraction of individual liability. The degree to which common risk variants represent “core” pathogenic insights is controversial. Individuals with rare and more penetrant risk variants are often intellectually disabled, which raises epistemological questions about classification. In clinical research, the application of polygenic risk scores—the cumulative sum of associated alleles in an individual genome—to prediction models of environmental influences and outcome is gaining enthusiasm because these scores explain more liability, but predictions are small and not yet actionable for individuals. Psychiatry is intertwined with genomic medicine, and our understanding of what we call schizophrenia and the possibilities of improving the lives of affected individuals have never seemed more promising. Yet the research challenges are daunting; psychiatric syndromes ultimately reflect how the brain mishandles environmental information, which at the systems level is far “downstream” of the effect of genes in cells.”

Weinberger DR: Thinking About Schizophrenia in an Era of Genomic Medicine. Amer. J. Psychiatry [Epub ahead of print, Jan.1,2019].


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Mitochondrial dysfunction has been implicated in a number of brain disorders. Traditionally, mitochondria and mitochondrial DNA (mtDNA) have been thought to be exclusively maternally inherited in humans. In this report, Luo and colleagues identified three unrelated multigeneration families with a high level of mtDNA heteroplasmy. A comprehensive exploration of mtDNA segregation in these families shows biparental mtDNA transmission with an autosomal dominant-like inheritance. The authors suggest that, while the central dogma of maternal inheritance of mtDNA remains valid, there are some exceptional cases where paternal mtDNA could be passed to the offspring.

Elucidating the molecular mechanism for this unusual mode of inheritance will provide new insights into how mtDNA is passed on from parent to offspring and may lead to development of new therapeutic treatments for pathogenic mtDNA transmission.

Luo S, Valencia CA, Zhang J, Lee NC, Slone J, Gui B, Wang X, Li Z, Dell S, Brown J, Chen SM, Chien YH, Hwu WL, Fan PC, Wong LJ, Atwal PS and Huang T: Biparental Inheritance of Mitochondrial DNA in Humans. Proc. Natl. Acad. Sci. USA 115(51): 13039-13044 (2018).


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Administration of the antidepressant fluoxetine to zebrafish, a common laboratory model, reduced levels of the stress hormone cortisol as well as exploratory behavior, effects that persisted across generations, according to a study by Vera-Chang and colleagues. They state that this may be a cause for concern given the high prescription rates of fluoxetine to pregnant women and the potential long-term negative impacts on humans exposed to these therapeutic drugs.

Vera-Chang MN, St-Jacques AD, Gagné R, Martyniuk CJ, Yauk CL, Moon TW and Trudeau VL: Transgenerational hypocortisolism and behavioral disruption are induced by the antidepressant fluoxetine in male zebrafish Danio rerio. Proc. Natl. Acad. Sci. USA 115(52):E12435-E12442 (2018).


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Cognitive impairment in major depressive disorder (MDD), including remitted major depressive disorder, raises the question whether these cognitive defects are part of preexisting vulnerability or a consequence of the disorder or its treatment. The purpose of this study was to compare (via meta-analysis) cognitive performance between individuals with and without family history of major depressive disorder.

.Across 284 measures of cognition in 54 non-overlapping samples including 3246 relatives of people with MDD and 5222 controls, relatives of people with MDD performed worse than controls across all measures of cognition. Domain-specific meta-analyses showed similar size of relative-control difference in most domains of cognition, including Full-Scale IQ, verbal intelligence, perceptual intelligence, memory, academic performance, and language.

The authors concluded that a general impairment in cognition is a feature of familial disposition for major depressive disorder. They suggest that cognition may contribute to early risk identification for depression and may represent a target for early intervention.

MacKenzie LE, Uher R and Pavolva B: Cognitive Performance in First-Degree Relatives of Individuals With vs Without Major Depressive Disorder: A Meta-analysis. JAMA Psychiatry [Epub ahead of print, Dec. 26, 2018; doi: 10.1001/jamapsychiatry.2018.3672.]


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“The ApoE ε4 allele is the most significant genetic risk factor for late-onset Alzheimer disease. The risk conferred by ε4, however, differs across populations, with populations of African ancestry showing lower ε4 risk compared to those of European or Asian ancestry. The cause of this heterogeneity in risk effect is currently unknown; it may be due to environmental or cultural factors correlated with ancestry, or it may be due to genetic variation local to the ApoE region that differs among populations.” To test these hypotheses, the authors analyzed ApoE genotypes and genome-wide array data in individuals from African American and Puerto Rican populations. They concluded that factors contributing to the lower risk effect in the ApoE gene ε4 allele are likely due to ancestry-specific genetic factors near ApoE rather than non-genetic ethnic, cultural, and environmental factors. Further exploration of these hypotheses may lead to novel, population-specific therapeutics and risk predictions.

Rajabli F, Feliciano BE, Celis K, Hamilton-Nelson KL, Whitehead PL, Adams LD, Bussies PL, Manrique CP, et al: Ancestral origin of ApoE  ε4 Alzheimer disease risk in Puerto Rican and African American populations. PLoS Genet. 2018 Dec 5;14(12):e1007791. doi: 10.1371/journal.pgen.1007791. eCollection 2018 Dec.


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