ORCID Profile
0000-0001-5619-1123
Current Organisation
Zentralinstitut für Seelische Gesundheit
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Publisher: Springer Science and Business Media LLC
Date: 04-03-2016
DOI: 10.1038/NRD.2016.28
Abstract: 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 in iduals 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.
Publisher: Springer Science and Business Media LLC
Date: 02-2016
DOI: 10.1038/NN.4228
Publisher: Springer Science and Business Media LLC
Date: 10-04-2005
DOI: 10.1038/NN1438
Abstract: Using multimodal neuroimaging in humans, we demonstrate specific interactions between prefrontal activity and midbrain dopaminergic synthesis. A common V(108/158)M substitution in the gene for catecholamine-O-methyltransferase (COMT), an important enzyme regulating prefrontal dopamine turnover, predicted reduced dopamine synthesis in midbrain and qualitatively affected the interaction with prefrontal cortex. These data implicate a dopaminergic tuning mechanism in prefrontal cortex and suggest a systems-level mechanism for cognitive and neuropsychiatric associations with COMT.
Publisher: Springer Science and Business Media LLC
Date: 03-10-2016
DOI: 10.1038/NN.4398
Publisher: Springer Science and Business Media LLC
Date: 14-05-2013
DOI: 10.1038/MP.2013.73
Publisher: Springer Science and Business Media LLC
Date: 14-08-2023
DOI: 10.1038/S41380-023-02202-Z
Abstract: Most mental disorders have a typical onset between 12 and 25 years of age, highlighting the importance of this period for the pathogenesis, diagnosis, and treatment of mental ill-health. This perspective addresses interactions between risk and protective factors and brain development as key pillars accounting for the emergence of psychopathology in youth. Moreover, we propose that novel approaches towards early diagnosis and interventions are required that reflect the evolution of emerging psychopathology, the importance of novel service models, and knowledge exchange between science and practitioners. Taken together, we propose a transformative early intervention paradigm for research and clinical care that could significantly enhance mental health in young people and initiate a shift towards the prevention of severe mental disorders.
Publisher: Springer Science and Business Media LLC
Date: 08-01-2014
Publisher: Elsevier BV
Date: 2016
Publisher: Elsevier BV
Date: 12-2014
Publisher: Springer Science and Business Media LLC
Date: 18-12-2013
DOI: 10.1038/NATURE12818
Abstract: In a small fraction of patients with schizophrenia or autism, alleles of copy-number variants (CNVs) in their genomes are probably the strongest factors contributing to the pathogenesis of the disease. These CNVs may provide an entry point for investigations into the mechanisms of brain function and dysfunction alike. They are not fully penetrant and offer an opportunity to study their effects separate from that of manifest disease. Here we show in an Icelandic s le that a few of the CNVs clearly alter fecundity (measured as the number of children by age 45). Furthermore, we use various tests of cognitive function to demonstrate that control subjects carrying the CNVs perform at a level that is between that of schizophrenia patients and population controls. The CNVs do not all affect the same cognitive domains, hence the cognitive deficits that drive or accompany the pathogenesis vary from one CNV to another. Controls carrying the chromosome 15q11.2 deletion between breakpoints 1 and 2 (15q11.2(BP1-BP2) deletion) have a history of dyslexia and dyscalculia, even after adjusting for IQ in the analysis, and the CNV only confers modest effects on other cognitive traits. The 15q11.2(BP1-BP2) deletion affects brain structure in a pattern consistent with both that observed during first-episode psychosis in schizophrenia and that of structural correlates in dyslexia.
Publisher: Longdom Group
Date: 2013
Publisher: American Psychiatric Association Publishing
Date: 12-2010
Publisher: Elsevier BV
Date: 2016
Publisher: Wiley
Date: 24-02-2005
DOI: 10.1002/ANA.20401
Abstract: We have recently identified mutations in a gene leucine-rich repeat kinase-2 (LRRK2), which cause autosomal dominant Parkinson's disease. Here, we describe two families with autosomal dominant Parkinson's disease caused by a LRRK2 G2019S mutation. We present here a clinical description of patients, including 6-(18)F-fluoro-L-dopa positron emission tomography and discuss the potential implications of this mutation, which alters a conserved residue in a domain required for kinase activation.
Publisher: Springer Science and Business Media LLC
Date: 15-04-2012
DOI: 10.1038/NG.2250
Publisher: Elsevier BV
Date: 12-2010
DOI: 10.1016/J.CONB.2010.09.008
Abstract: Recent large-scale genetic studies have provided robust evidence implicating several novel susceptibility genes for schizophrenia. These include ZNF804A, TCF4 and NRGN, which contain common variants that weakly increase schizophrenia susceptibility, and NRXN1, in which rare copy number variants have a greater impact on schizophrenia risk. Investigation of these and other substantiated susceptibility genes are providing valuable insight into the primary neurobiological mechanisms underlying schizophrenia, which may lead to novel therapeutic interventions for the disorder. In the meantime, several novel pharmacological strategies, including activation of mGluRs, elevation of synaptic glycine and inhibition of phosphodiesterase 10A, have recently shown promise for the treatment of schizophrenia in clinical trials.
Publisher: Springer Science and Business Media LLC
Date: 21-01-2015
DOI: 10.1038/NATURE14101
Publisher: Informa UK Limited
Date: 22-03-2018
DOI: 10.1080/15622975.2018.1449966
Abstract: Epidemiological and experimental evidence suggests that the endocannabinoid system plays a pathophysiological role in schizophrenia. This is reflected by elevated cerebrospinal levels of the endocannabinoid anandamide in schizophrenia and its initial prodromal states. We analyzed plasma concentrations of anandamide, 2-arachidonoyl-sn-glycerol, palmitoylethanolamide and oleoylethanolamide from 25 twin pairs discordant for schizophrenia, six discordant for bipolar disorder and eight healthy twin pairs to determine hereditary traits. Twin pairs discordant for schizophrenia or bipolar disorder had significantly higher levels of anandamide and palmitoylethanolamide compared to healthy twins (both P < 0.002). Non-affected twins discordant for schizophrenia, who developed a psychotic disorder within 5 years follow-up showed lower anandamide (P = 0.042) and 2-arachidonoyl-sn-glycerol levels (P = 0.049) than twins who remained healthy. We suggest that the protective upregulation of endocannabinoid signalling reflects either a hereditary trait or mirrors a modulating response to genetically influenced cerebral function involving, e.g., other neurotransmitters or energy metabolism.
Publisher: American Medical Association (AMA)
Date: 11-2014
DOI: 10.1001/JAMAPSYCHIATRY.2014.1215
Abstract: Obesity has emerged as a leading health threat but its biological basis remains insufficiently known, h ering the search for novel treatments. Here, we study oleoylethanolamide, a naturally occurring lipid that has been clearly implicated in weight regulation in animals. However, its role for weight regulation and obesity in humans is still unclear. To investigate associations between plasma oleoylethanolamide levels and body mass index (BMI, calculated as weight in kilograms ided by height in meters squared) and functional magnetic resonance imaging response to food stimuli in obese patients and matched control participants. Case-control study of 21 obese patients and 24 matched control participants. Obesity was defined as having a BMI of at least 30. The mean age of participants was 40.8 years and BMIs ranged from 18.2 to 47.5. Interactions between plasma oleoylethanolamide levels and obesity on BMI and functional magnetic resonance imaging response to food stimuli. Associations between oleoylethanolamide and BMI differed significantly depending on whether in iduals were obese or not (P = .02). In obese in iduals, oleoylethanolamide showed a trend toward a positive correlation with BMI (P = .06, ρ = 0.42), while this relationship was inverse for nonobese control participants (P = .07, ρ = -0.34). Similarly, we found significant interactions between oleoylethanolamide levels and obesity on food-related brain activation in cortical areas associated with reward processing and interoceptive signaling (P = .009). Specifically, nonobese in iduals with higher oleoylethanolamide levels had higher insular brain activity (P < .001, ρ = 0.70) again, the relationship trended to be inverse for obese patients (P = .11, ρ = -0.36). These effects were not associated with plasma levels of leptin and anandamide, suggesting an independent role of oleoylethanolamide in hunger-associated interoceptive signaling. Analysis of food craving during the functional magnetic resonance imaging task suggested that the identified brain areas may be involved in suppressing food-liking reactions in nonobese in iduals. This study suggests that oleoylethanolamide-mediated signaling plays an important role for hedonic regulation of food craving and obesity in humans and thus may be a valuable target for developing novel antiobesity drugs.
Publisher: Oxford University Press (OUP)
Date: 24-05-2014
Publisher: Springer Science and Business Media LLC
Date: 09-04-2013
DOI: 10.1038/MP.2013.37
Location: United States of America
No related grants have been discovered for Andreas Meyer-Lindenberg.