Volume 26, Issue 6

Magnetic resonance spectroscopy (MRS) provides unique information about the neurobiological substrates of brain function in health and disease. However, many of the physical principles underlying MRS are distinct from those underlying magnetic resonance imaging, and they may not be widely understood by neuroscientists new to this methodology. This review describes these physical principles and many of the technical methods in current use for MRS experiments. A better understanding these principles and methods may help investigators select pulse sequences and quantification methods best suited to the aims of their research program and avoid pitfalls that can hamper new investigators in this field.

Physicians and scientists can use fractal analysis as a tool to objectively quantify complex patterns found in neuroscience and neurology. Fractal analysis has the potential to allow physicians to make predictions about clinical outcomes, categorize pathological states, and eventually generate diagnoses. In this review, we categorize and analyze the applications of fractal theory in neuroscience found in the literature. We discuss how fractals are applied and what evidence exists for fractal analysis in neurodegeneration, neoplasm, neurodevelopment, neurophysiology, epilepsy, neuropharmacology, and cell morphology. The goal of this review is to introduce the medical community to the utility of applying fractal theory in clinical neuroscience.

In recent years, multiple studies have shown task-induced negative blood-oxygenation-level-dependent responses (NBRs) in multiple brain regions in humans and animals. Converging evidence suggests that task-induced NBRs can be interpreted in terms of decreased neuronal activity. However, the vascular and metabolic dynamics and functional importance of the NBR are highly debated. Here, we review studies investigating the origin and functional importance of the NBR, with special attention to the somatosensory cortex.

Electric foot shock is a complex stressor with both physical and emotional components. It has been employed as an important tool to develop diverse animal models in the field of psychopharmacology. The electric foot shock paradigm includes acute or chronic exposures of shocks of varying intensity and duration on an electrified grid floor in an electric foot shock apparatus. Research evidence reveals that foot shocks of varying intensity produce behavioral and neurochemical changes reflecting depression, anxiety, and post-traumatic stress disorder (PTSD) in humans. Animals generally do not habituate to foot shocks in comparison to other stressors, including loud noise, bright light, and hot and cold temperatures. Additionally, it offers an experimental advantage of control over intensity and duration; therefore, by varying its application parameters, different disorder models have been created. Electric foot shock fear conditioning-induced ultrasonic vocalization and fear-potentiated startle have been explored to develop models of anxiety and panic. Similarly, fear conditioning in the form of foot shock exposure followed by situational reminders has been used to develop a model of PTSD. Electric foot shock-induced conflict has been explored to develop operant conflict models (Geller-Seifter and Vogel tests), which in turn are pharmacologically validated to screen potential anti-anxiety agents. Inescapable electric shock-induced ‘learned helplessness’ mimics the symptomology of depression, and this phenomenon has been employed to develop the model of depression. The present review describes the pharmacologically validated models of anxiety, depression, and PTSD involving electric foot shock as an aversive stimulus.

Seasonal affective disorder (SAD) is characterized by recurrent depression occurring generally in fall/winter. Numerous pieces of evidence indicate the association of SAD with decreased brain neurotransmitter serotonin (5-HT) system functioning. Tryptophan hydroxylase 2 (TPH2) is the key and rate-limiting enzyme in 5-HT synthesis in the brain. This paper concentrates on the relationship between TPH2 activity and mood disturbances, the association between human TPH2 gene expression and the risk of affective disorder, application of tryptophan to SAD treatment and the animal models of SAD. The main conclusions of this review are as follows: (i) the brain 5-HT deficiency contributes to the mechanism underlying SAD, (ii) TPH2 is involved in the regulation of some kinds of genetically defined affective disorders and (iii) the activation of 5-HT synthesis with exogenous l -tryptophan alone or in combination with light therapy could be effective in SAD treatment. The synergic effect of these combined treatments will have several advantages compared to light or tryptophan therapy alone. First, it is effective in the treatment of patients resistant to light therapy. Secondly, l -tryptophan treatment prolongs the antidepressant effect of light therapy.

This review, for the first time, aims to summarize the current knowledge in the emerging field of RAGE (receptor for advanced glycation end-products) studies in neurodegeneration and neurodegenerative diseases. RAGE, a member of the multiligand cell surface immunoglobulin family, has been implicated in numerous pathological conditions – from diabetes and cardiovascular diseases to tumors and neurodegenerative disorders, such as Alzheimer’s disease, familial amyloid polyneuropathy, diabetic neuropathy, Parkinson’s disease, and Huntington’s disease. Until now, the detailed mechanisms of the contribution of RAGE to neurodegeneration remain elusive; however, mounting evidence suggests that its detrimental actions are triggered by its ligand interactions and contribute to increased neuroinflammation, neuronal degeneration, and apoptosis. Deciphering the role of RAGE in neurodegenerative disorders will be a milestone in our basic understanding of the mechanisms involved in the pathogenesis of neurodegeneration, helping to delineate molecular links between complex RAGE signaling pathways and neuronal dysfunction and neurodegeneration.

Depression is a major mental disease that is ranked as the fourth leading cause of disability. In order to avoid unwanted adverse reactions, as well as improve efficacy, current researches are seeking alternatives to conventional antidepressants. Phytochemicals provide an extensive research area in antidepressant therapies. The aim of the present study is to comprehensively review neurological evidences demonstrating the efficacy of phytochemicals in depression. For this purpose, electronic databases were searched to collect all data on the antidepressant mechanisms of phytochemicals from 1966 up to 2015. Plant metabolites from different categories including polyphenols (flavonoids, phenolic acids, lignanes, coumarins), alkaloids, terpenes and terpenoids, saponins and sapogenins, amines, and carbohydrates were found to possess antidepressant activity. Naringenin, quercetin derivatives, eugenol, piperine, diterpene alkaloids, berberine, hyperforin, riparin derivatives, ginsenosides, as well as β-carboline alkaloids are among the most relevant ones. Naringenin has represented its antidepressant effect by elevation of serotonin (5-HT), norepinephrine, brain-derived neurotrophic factor (BDNF), and glucocorticoid receptors. Piperine demonstrated inhibition of monoamine oxidase enzymes, elevation of brain 5-HT and BDNF levels, and modulation of the hypothalamus-pituitary-adrenal axis. The serotonergic, noradrenergic, and dopaminergic effect of berberine has been proven in several studies. Quercetin derivatives have revealed antidepressant potential via elevating pro-opiomelanocortin and neuroprotective properties, as well as reduction of proinflammatory cytokines. Assessing the structure-activity relationship of highly potent antidepressant phytochemicals is suggested to find future natural, semisynthetic, or synthetic antidepressants. Further clinical studies are also necessary for confirmation of natural antidepressant efficacy and completion of their safety profile.

For the past three and a half decades, the Psychopathy Checklist-Revised (PCL-R) and the self-report Psychopathic Personality Inventory-Revised (PPI-R) have been the standard measures for the diagnosis of psychopathy. Technological approaches can enhance these diagnostic methodologies. The purpose of this paper is to present a state-of-the-art review of various technological approaches for spotting psychopathy, such as electroencephalogram (EEG), magnetic resonance imaging (MRI), functional MRI (fMRI), transcranial magnetic stimulation (TMS), and other measures. Results of EEG event-related potential (ERP) experiments support the theory that impaired amygdala function may be responsible for abnormal fear processing in psychopathy, which can ultimately manifest as psychopathic traits, as outlined by the PCL-R or PPI-R. Imaging studies, in general, point to reduced fear processing capabilities in psychopathic individuals. While the human element, introduced through researcher/participant interactions, can be argued as unequivocally necessary for diagnosis, these purely objective technological approaches have proven to be useful in conjunction with the subjective interviewing and questionnaire methods for differentiating psychopaths from non-psychopaths. Furthermore, these technologies are more robust than behavioral measures, which have been shown to fail.