Reduced speech coherence in psychosis-related social media forum posts.

The extraction of linguistic markers from social media posts, which are indicative of the onset and course of mental disorders, offers great potential for mental healthcare. In the present study, we extracted over one million posts from the popular social media platform Reddit to analyze speech coherence, which reflects formal thought disorder and is a characteristic feature of schizophrenia and associated psychotic disorders. Natural language processing (NLP) models were used to perform an automated quantification of speech coherence. We could demonstrate that users who are active on forums geared towards disorders with a higher degree of psychotic symptoms tend to show a lower level of coherence. The lowest coherence scores were found in users of forums on dissociative identity disorder, schizophrenia, and bipolar disorder. In contrast, a relatively high level of coherence was detected in users of forums related to obsessive-compulsive disorder, anxiety, and depression. Users of forums on posttraumatic stress disorder, autism, and attention-deficit hyperactivity disorder exhibited medium-level coherence. Our findings provide promising first evidence for the possible utility of NLP-based coherence analyses for the early detection and prevention of psychosis on the basis of posts gathered from publicly available social media data. This opens new avenues for large-scale prevention programs aimed at high-risk populations.

A fatal alliance: Glial connexins, myelin pathology and mental disorders.

Mature oligodendrocytes are myelin forming glial cells which are responsible for myelination of neuronal axons in the white matter of the central nervous system. Myelin pathology is a major feature of severe neurological disorders. Oligodendrocyte-specific gene mutations and/or white matter alterations have also been addressed in a variety of mental disorders. Breakdown of myelin integrity and demyelination is associated with severe symptoms, including impairments in motor coordination, breathing, dysarthria, perception (vision and hearing), and cognition. Furthermore, there is evidence indicating that myelin sheath defects and white matter pathology contributes to the affective and cognitive symptoms of patients with mental disorders. Oligodendrocytes express the connexins GJC2; mCx47 [human (GJC2) and mouse (mCx47) connexin gene nomenclature according to Söhl and Willecke (2003)], GJB1; mCx32, and GJD1; mCx29 in both white and gray matter. Preclinical findings indicate that alterations in connexin expression in oligodendrocytes and astrocytes can induce myelin defects. GJC2; mCx47 is expressed at early embryonic stages in oligodendrocyte precursors cells which precedes central nervous system myelination. In adult humans and animals GJC2, respectively mCx47 expression is essential for oligodendrocyte function and ensures adequate myelination as well as myelin maintenance in the central nervous system. In the past decade, evidence has accumulated suggesting that mental disorders can be accompanied by changes in connexin expression, myelin sheath defects and corresponding white matter alterations. This dual pathology could compromise inter-neuronal information transfer, processing and communication and eventually contribute to behavioral, sensory-motor, affective and cognitive symptoms in patients with mental disorders. The induction of myelin repair and remyelination in the central nervous system of patients with mental disorders could help to restore normal neuronal information propagation and ameliorate behavioral and cognitive symptoms in individuals with mental disorders.

A new path to mental disorders: Through gap junction channels and hemichannels.

Behavioral disturbances related to emotional regulation, reward processing, cognition, sleep-wake regulation and activity/movement represent core symptoms of most common mental disorders. Increasing empirical and theoretical evidence suggests that normal functioning of these behavioral domains relies on fine graded coordination of neural and glial networks which are maintained and modulated by intercellular gap junction channels and unapposed pannexin or connexin hemichannels. Dysfunctions in these networks might contribute to the development and maintenance of psychopathological and neurobiological features associated with mental disorders. Here we review and discuss the evidence indicating a prominent role of gap junction channel and hemichannel dysfunction in core symptoms of mental disorders. We further discuss how the increasing knowledge on intercellular gap junction channels and unapposed pannexin or connexin hemichannels in the brain might lead to deeper mechanistic insight in common mental disorders and to the development of novel treatment approaches. We further attempt to exemplify what type of future research on this topic could be integrated into multidimensional approaches to understand and cure mental disorders.

Recognition memory, primacy vs. recency effects, and time perception in the online version of the fear of scream paradigm.

Anxiety disorders are characterized by cognitive dysfunctions which contribute to the patient's profound disabilities. The threat of shock paradigm represents a validated psychopathological model of anxiety to measure the impact of anxiety on cognitive processes. We have developed an online version of the threat of scream paradigm (ToSP) to investigate the impact of experimental anxiety on recognition memory. Two animated passive walkthrough videos (either under threat of scream or safety conditions) were shown to healthy participants. Recognition memory, primacy vs. recency effects, and subjective estimations of the length of encoding sessions were assessed. Subjective anxiety, stress, and emotional arousal ratings indicated that experimental anxiety could successfully be induced (Safe-Threat) or reversed (Threat-Safe) between the two passive walkthrough sessions. Participants exposed to distress screams showed impaired retrieval of complex information that has been presented in an animated environment. In the threat condition, participants failed to recognize details related to the persons encountered, their spatial locations, as well as information about the temporal order and sequence of encounters. Participant groups, which received a threat announcement prior to the first walkthrough session (Threat-Threat vs. Safety-Safety and Threat-Safety vs. Safety-Threat) showed poorer recognition memory as compared to the groups that received a safety announcement (P = 0.0468 and P = 0.0426, respectively; Mann-Whitney U test, Cohen's d = 0.5071; effect size r = 0.2458). In conclusion, experimental anxiety induced by the online version of the ToSP leads to compromised recognition memory for complex multi-dimensional information. Our results indicate that cognitive functions of vulnerable populations (with limited mobility) can be evaluated online by means of the ToSP.