Band 28, Heft 4

Unlike any other species, humans frequently engage in altruistic behaviors by which they increase another individual’s welfare even if this implies personal costs. The psychological motives underlying altruistic behaviors remain diverse, ranging from the ability to reciprocate trust and cooperation to bonding and empathizing with family members or even genetically unrelated others. This article explores the neuroendocrine architecture of altruism by emphasizing the crucial role of the evolutionarily highly conserved peptide hormone oxytocin as a modulator of cooperative behaviors including empathy-driven altruism. However, accumulating evidence suggests that oxytocin does not invariably facilitate cooperation but also produces protective or even defensive-aggressive responses in specific social contexts. In addition, we highlight the relevance of message frames as critical determinants of whether the peptide promotes altruism toward prosocial ends.

Theories of human mental abilities should be consistent with what is known in neuroscience. Currently, tests of human mental abilities are modeled by cognitive constructs such as attention, working memory, and speed of information processing. These constructs are in turn related to a single general ability. However, brains are very complex systems and whether most of the variability between the operations of different brains can be ascribed to a single factor is questionable. Research in neuroscience suggests that psychological processes such as perception, attention, decision, and executive control are emergent properties of interacting distributed networks. The modules that make up these networks use similar computational processes that involve multiple forms of neural plasticity, each having different time constants. Accordingly, these networks might best be characterized in terms of the information they process rather than in terms of abstract psychological processes such as working memory and executive control.

The mitochondria of different cells are different in their morphological and biochemical properties. These organelles generate free radicals during activity, leading inevitably to mitochondrial DNA damage. It is not clear how this problem is addressed in long-lived cells, such as neurons. We propose the hypothesis that mitochondria within the same cell also differ in lifespan and ability to divide. According to our suggestion, cells have a pool of ‘stem’ mitochondria with low metabolic activity and a pool of ‘differentiated’ mitochondria with significantly shorter lifespans and high metabolic activity. We consider synaptic mitochondria as a possible example of ‘differentiated’ mitochondria. They are significantly smaller than mitochondria from the cell body, and they are different in key enzyme activity levels, proteome, and lipidome. Synaptic mitochondria are more sensitive to different damaging factors. It has been established that neurons have a sorting mechanism that sends mitochondria with high membrane potential to presynaptic endings. This review describes the properties of synaptic mitochondria and their role in the regulation of synaptic transmission.

The current grade classification system of gliomas is based on the histopathological features of these tumors and has great significance in defining groups of patients for clinical assessment. However, this classification system is also associated with a number of limitations, and as such, additional clinical assessment criteria are required. Long non-coding RNAs (lncRNAs) play a critical role in cellular functions and are currently regarded as potential biomarkers for glioma diagnosis and prognosis. Therefore, the molecular classification of glioma based on lncRNA expression may provide additional information to assist in the systematic identification of glioma. In the present paper, we review the emerging evidence indicating that specific lncRNAs may have the potential for use as key novel biomarkers and thus provide a powerful tool for the systematic diagnosis of glioma.

Upregulation of defensive reflexes such as the nociceptive flexion reflex (NFR) has been attributed to sensitisation of peripheral and spinal nociceptors and is often considered biomarkers of pain. Experimental modulation of defensive reflexes raises the possibility that they might be better conceptualised as markers of descending cognitive control. Despite strongly held views on both sides and several narrative reviews, there has been no attempt to evaluate the evidence in a systematic manner. We undertook a meta-analytical systematic review of the extant English-language literature from inception. Thirty-six studies satisfied our a priori criteria. Seventeen were included in the meta-analysis. Reflexive threshold was lower in people with clinical pain than it was in pain-free controls, but reflex size, latency, and duration were unaffected. The pattern of difference was not consistent with sensitisation of nociceptive neurones, as these changes were not isolated to the affected body part but was more consistent with top-down cognitive control reflective of heightened protection of body tissue. The pattern of modulation is dependent on potentially complex evaluative mechanisms. We offer recommendations for future investigations and suggest that defensive reflex threshold may reflect a biomarker of a broader psychological construct related to bodily protection, rather than sensitisation of primary nociceptors, spinal nociceptors, or pain.

Adult neurogenesis is one of the most important mechanisms contributing to brain development, learning, and memory. Alterations in neurogenesis underlie a wide spectrum of brain diseases. Neurogenesis takes place in highly specialized neurogenic niches. The concept of neurogenic niches is becoming widely accepted due to growing evidence of the important role of the microenvironment established in the close vicinity to stem cells in order to provide adequate control of cell proliferation, differentiation, and apoptosis. Neurogenic niches represent the platform for tight integration of neurogenesis and angiogenesis supported by specific properties of cerebral microvessel endothelial cells contributing to establishment of partially compromised blood-brain barrier (BBB) for the adjustment of local conditions to the current metabolic needs of stem and progenitor cells. Here, we review up-to-date data on microvascular dynamics in activity-dependent neurogenesis, specific properties of BBB in neurogenic niches, endothelial-driven mechanisms of clonogenic activity, and future perspectives for reconstructing the neurogenic niches in vitro .

Given that achievement in learning mathematics at school correlates with work and social achievements, it is important to understand the cognitive processes underlying abilities to learn mathematics efficiently as well as reasons underlying the occurrence of mathematics anxiety (i.e. feelings of tension and fear upon facing mathematical problems or numbers) among certain individuals. Over the last two decades, many studies have shown that learning mathematical and numerical concepts relies on many cognitive processes, including working memory, spatial skills, and linguistic abilities. In this review, we discuss the relationship between mathematical learning and cognitive processes as well as the neural substrates underlying successful mathematical learning and problem solving. More importantly, we also discuss the relationship between these cognitive processes, mathematics anxiety, and mathematics learning disabilities (dyscalculia). Our review shows that mathematical cognition relies on a complex brain network, and dysfunction to different segments of this network leads to varying manifestations of mathematical learning disabilities.

Emotion dysregulation is a frequent feature in trauma-related disorders. Different kinds of emotion dysregulation seem to be linked to particular psychiatric conditions, and there is growing evidence of the association between neurobiological correlates and those dysregulation patterns. Nevertheless, many of the recent findings from the field of the neurobiology have not been translated into clinical practice and are insufficiently contemplated in trauma-oriented therapies. The aim of this article is to review recent developments in the field of emotion regulation connecting these issue with the practical implementation of psychotherapeutic procedures. The evaluation of emotion dysregulation patterns can guide decision making during the therapy independently to the approach, but there are some findings that can be especially useful for some concrete modalities of therapy. In this article we will focus our discussion on how emotion dysregulation may influence eye movement desensitization and reprocessing (EMDR) treatment in trauma-related disorders. EMDR is a well-defined and protocol-based intervention, with a strong empirical support for post-traumatic stress disorder (PTSD). We describe how different patterns of emotion dysregulation may influence EMDR treatment and procedures, and also how the application of EMDR beyond non-dissociative PTSD should take into account the predominant emotion-regulation strategies in specific posttraumatic disorders.

Major depressive disorder is a common debilitating mood disorder that affects quality of life. Prefrontal cortex abnormalities, an imbalance in neurotransmitters, neuroinflammation, and mitochondrial dysfunction are the major factors in the etiology of major depressive disorder. Despite the efficacy of pharmacotherapy in the treatment of major depressive disorder, 30%–40% of patients do not respond to antidepressants. Given this, exploring the alternative therapies for treatment or prevention of major depressive disorder has aroused interest among scientists. Transcranial photobiomodulation therapy is the use of low-power lasers and light-emitting diodes in the far-red to near-infrared optical region for stimulation of neuronal activities. This non-invasive modality improves the metabolic capacity of neurons due to more oxygen consumption and ATP production. Beneficial effects of transcranial photobiomodulation therapy in the wide range of neurological and psychological disorders have been already shown. In this review, we focus on some issue relating to the application of photobiomodulation therapy for major depressive disorder. There is some evidence that transcranial photobiomodulation therapy using near-infrared light on 10-Hz pulsed mode appears to be a hopeful technique for treatment of major depressive disorder. However, further studies are necessary to find the safety of this method and to determine its effective treatment protocol.