Volume 33, Issue 1

The microtubule-associated protein (MAP) TAU is mainly sorted into the axon of healthy brain neurons. Somatodendritic missorting of TAU is a pathological hallmark of many neurodegenerative diseases, including Alzheimer’s disease (AD). Cause, consequence and (patho)physiological mechanisms of TAU sorting and missorting are understudied, in part also because of the lack of readily available human neuronal model systems. The human neuroblastoma cell line SH-SY5Y is widely used for studying TAU physiology and TAU-related pathology in AD and related tauopathies. SH-SY5Y cells can be differentiated into neuron-like cells (SH-SY5Y-derived neurons) using various substances. This review evaluates whether SH-SY5Y-derived neurons are a suitable model for (i) investigating intracellular TAU sorting in general, and (ii) with respect to neuron subtype-specific TAU vulnerability. (I) SH-SY5Y-derived neurons show pronounced axodendritic polarity, high levels of axonally localized TAU protein, expression of all six human brain isoforms and TAU phosphorylation similar to the human brain. As SH-SY5Y cells are highly proliferative and readily accessible for genetic engineering, stable transgene integration and leading-edge genome editing are feasible. (II) SH-SY5Y-derived neurons display features of subcortical neurons early affected in many tauopathies. This allows analyzing brain region-specific differences in TAU physiology, also in the context of differential vulnerability to TAU pathology. However, several limitations should be considered when using SH-SY5Y-derived neurons, e.g., the lack of clearly defined neuronal subtypes, or the difficulty of mimicking age-related tauopathy risk factors in vitro . In brief, this review discusses the suitability of SH-SY5Y-derived neurons for investigating TAU (mis)sorting mechanisms and neuron-specific TAU vulnerability in disease paradigms.

The auditory mismatch negativity, a component of the event-related potential elicited by an unexpected stimulus in a sequence of acoustic stimuli, provides an objective measure of the accuracy of the echoic information processing of the human brain in vivo . Auditory mismatch negativity is also a useful probe of cortical glutamatergic N -methyl- d -aspartate receptor activity and disturbance. Notably, auditory mismatch negativity is consistently impaired in schizophrenia. Because of the wide spectrum extending from bipolar affective illness and schizoaffective psychosis to typical schizophrenia, we examined the literature on auditory mismatch negativity in bipolar disorder with the aim to find any neurophysiological dysfunction concerning pre-attentive information processing shared by these clinical conditions. This focused review includes 26 original articles published in peer-reviewed journals and indexed in the National Institutes of Health National Library of Medicine (PubMed) search system. Overall, evidence is consistent with the finding that auditory mismatch negativity is impaired in bipolar disorder with psychotic features, even though to a lesser extent than in schizophrenia. It must be acknowledged that, in a few twin and family studies, mismatch negativity abnormalities were not specifically associated with bipolar disorder. In conclusion, auditory mismatch negativity research supports the involvement of the N-methyl- d -aspartate system in the pathophysiology of bipolar disorder, as previously assessed for schizophrenia, thus creating an intriguing trait d’union between these two mental illnesses and stimulating the development of novel therapeutic agents. With additional replication and validation, auditory mismatch negativity may be further considered as a correlate of a common psychopathology of schizophrenia and bipolar spectrum illnesses.

There has been an enormous amount of interest in how the brain seeks information. The study of this issue is a rapidly growing field in neuroscience. Information seeking is to make informative choices among multiple alternatives. A central issue in information seeking is how the value of information is assessed in order to choose informative alternatives. This issue has been studied in psychology, economics, and artificial intelligence. The present review is focused on information assessment and summarizes the psychological and computational criteria with which humans and computers assess information. Based on the summary, neurophysiological findings are discussed. In addition, a computational view of the relationships between these criteria is presented.

Empathy is essential for navigating complex social environments. Prior work has shown associations between rs53576, a single nucleotide polymorphism (SNP) located in the oxytocin receptor gene ( OXTR ), and generalized empathy. We undertook a systematic review and meta-analysis to assess the effects of rs53576 on subdomains of empathy, specifically cognitive empathy (CE) and affective empathy (AE), in healthy adults. Twenty cohorts of 8933 participants aged 18–98 were identified, including data from the Sydney Memory and Ageing Study, a cohort of older community adults. Meta-analyses found G homozygotes had greater generalized empathic abilities only in young to middle-aged adults. While meta-analyses of empathy subdomains yielded no significant overall effects, there were differential effects based on ethnicity. G homozygotes were associated with greater CE abilities in Asian cohorts (standardized mean difference; SMD: 0.09 [2.8·10 −3 –0.18]), and greater AE performance in European cohorts [SMD: 0.12 (0.04–0.21)]. The current literature highlights a need for further work that distinguishes between genetic and ethnocultural effects and explores effects of advanced age on this relationship.

Major depressive disorder is a genetic susceptible disease, and a psychiatric syndrome with a high rate of incidence and recurrence. Because of its complexity concerning etiology and pathogenesis, the cure rate of first-line antidepressants is low. In recent years, accumulative evidences revealed that oxytocin act as a physiological or pathological participant in a variety of complex neuropsychological activities, including major depressive disorder. Six electronic databases (Web of Science, PubMed, Scopus, Google Scholar, CNKI, and Wanfang) were employed for researching relevant publications. At last, 226 articles were extracted. The current review addresses the correlation of the oxytocin system and major depressive disorder. Besides, we summarize the mechanisms by which the oxytocin system exerts potential antidepressant effects, including regulating neuronal activity, influencing neuroplasticity and regeneration, altering neurotransmitter release, down regulating hypothalamic–pituitary–adrenal axis, anti-inflammatory, antioxidation, and genetic effects. Increasing evidence shows that oxytocin and its receptor gene may play a potential role in major depressive disorder. Future research should focus on the predictive ability of the oxytocin system as a biomarker, as well as its role in targeted prevention and early intervention of major depressive disorder.

Coronavirus disease 2019 (COVID-19) is an infectious respiratory disease, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Evidence-based emerging reports of neurological manifestations show that SARS-CoV-2 can attack the nervous system. However, little is known about the biomarkers in disease in neuropsychiatric and neuroimmunological disorders. One of the important keys in the management of COVID-19 is an accurate diagnosis. Biomarkers could provide valuable information in the early detection of disease etiology, diagnosis, further treatment, and prognosis. Moreover, ongoing investigations on hematologic, biochemical, and immunologic biomarkers in nonsevere, severe, or fatal forms of COVID-19 patients provide an urgent need for the identification of clinical and laboratory predictors. In addition, several cytokines acting through mechanisms to emerge immune response against SARS-CoV-2 infection are known to play a major role in neuroinflammation. Considering the neuroinvasive potential of SARS-CoV-2, which can be capable of triggering a cytokine storm, the current evidence on inflammation in psychiatry and neurodegenerative by emerging neuroinflammation is discussed in this review. We also highlighted the hematologic, biochemical, and immunologic biomarkers in COVID-19 diagnosis. COVID-19 prognostic biomarkers in patients with neuropsychiatric and neuroimmunological diseases are also explained.

Circadian rhythms in most living organisms are regulated by light and synchronized to an endogenous biological clock. The circadian clock machinery is also critically involved in regulating and fine-tuning neurodevelopmental processes. Circadian disruption during embryonic development can impair crucial phases of neurodevelopment. This can contribute to neurodevelopmental disorders like autism spectrum disorder (ASD) in the offspring. Increasing evidence from studies showing abnormalities in sleep and melatonin as well as genetic and epigenetic changes in the core elements of the circadian pathway indicate a pivotal role of circadian disruption in ASD. However, the underlying mechanistic basis through which the circadian pathways influence the risk and progression of ASD are yet to be fully discerned. Well-recognized mechanistic pathways in ASD include altered immune-inflammatory, nitro oxidative stress, neurotransmission and synaptic plasticity, and metabolic pathways. Notably, all these pathways are under the control of the circadian clock. It is thus likely that a disrupted circadian clock will affect the functioning of these pathways. Herein, we highlight the possible mechanisms through which aberrations in the circadian clock might affect immune-inflammatory, nitro-oxidative, metabolic pathways, and neurotransmission, thereby driving the neurobiological sequelae leading to ASD.