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Just before 2020 began, a novel coronavirus, severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), brought for humans a potentially fatal disease known as coronavirus disease 2019 (COVID-19). The world has thoroughly been affected by COVID-19, while there has been little progress towards understanding the pathogenesis of COVID-19. Patients with a severe phenotype of disease and those who died from the disease have shown hyperinflammation and were more likely to develop neurological manifestations, linking the clinical disease with neuroimmunological features. Anosmia frequently occurs early in the course of COVID-19. The prevalence of anosmia would be influenced by self-diagnosis as well as self-misdiagnosis in patients with COVID-19. Despite this, the association between anosmia and COVID-19 has been a hope for research, aiming to understand the pathogenesis of COVID-19. Studies have suggested differently probable mechanisms for the development of anosmia in COVID-19, including olfactory cleft syndrome, postviral anosmia syndrome, cytokine storm, direct damage of olfactory sensory neurons, and impairment of the olfactory perception center in the brain. Thus, the observation of anosmia would direct us to find the pathogenesis of COVID-19 in the central nervous system, and this is consistent with numerous neurological manifestations related to COVID-19. Like other neurotropic viruses, SARS-CoV-2 might be able to enter the central nervous system via the olfactory epithelium and induce innate immune responses at the site of entry. Viral replication in the nonneural olfactory cells indirectly causes damage to the olfactory receptor nerves, and as a consequence, anosmia occurs. Further studies are required to investigate the neuroimmunology of COVID-19 in relation to anosmia.

Major depressive disorder (MDD) symptoms commonly occur after trauma-exposure, both alone and in combination with post-traumatic stress disorder (PTSD). This article reviews recent research on comorbidity between these disorders, including its implications for symptom severity and response to treatment. Despite considerable symptom overlap, the two disorders represent distinct constructs and depend, at least in part, on separate biological mechanisms. Both, however, are also clearly related to stress psychopathology. We recommend that more research focus specifically on the study of individual differences in symptom expression in order to identify distinct subgroups of individuals and develop targeted treatments. However, a barrier to this line of inquiry is the trend of excluding particular patients from clinical trials of new interventions based on symptom severity or comorbidity. Another obstacle is the overreliance on self-report measures in human research. We argue that developing computer-based behavioral measures in order to supplement self-report can help address this challenge. Furthermore, we propose that these measures can help tie findings from human and non-human animal research. A number of paradigms have been used to model MDD-and PTSD-like behavior in animals. These models remain valuable for understanding the biological basis of these disorders in humans and for identifying potential interventions, but they have been underused for the study of comorbidity. Although the interpretation of animal behavior remains a concern, we propose that this can also be overcome through the development of close human analogs to animal paradigms.

While the “physiological” aging process is associated with declines in motor and cognitive features, these changes do not significantly impair functions and activities of daily living. Differently, motor and cognitive impairment constitute the most common phenotypic expressions of neurodegeneration. Both manifestations frequently coexist in the same disease, thus making difficult to detect “pure” motor or cognitive conditions. Movement disorders are often characterized by cognitive disturbances, and neurodegenerative dementias often exhibit the occurrence of movement disorders. Such a phenotypic overlap suggests approaching these conditions by highlighting the commonalities of entities traditionally considered distinct. In the present review, we critically reappraised the common clinical and pathophysiological aspects of neurodegeneration in both animal models and patients, looking at motricity as a trait d’union over the spectrum of neurodegeneration and focusing on synaptopathy and oscillopathy as the common pathogenic background. Finally, we discussed the possible role of movement as neuroprotective intervention in neurodegenerative conditions, regardless of the etiology. The identification of commonalities is critical to drive future research and develop novel possible disease-modifying interventions.

Central nervous system (CNS) diseases are common diseases that threaten human health. The CNS is highly enriched in lipids, which play important roles in maintaining normal physiological functions of the nervous system. Moreover, many CNS diseases are closely associated with abnormal lipid metabolism. Exosomes are a subtype of extracellular vesicles (EVs) secreted from multivesicular bodies (MVBs) . Through novel forms of intercellular communication, exosomes secreted by brain cells can mediate inter-neuronal signaling and play important roles in the pathogenesis of CNS diseases. Lipids are essential components of exosomes, with cholesterol and sphingolipid as representative constituents of its bilayer membrane. In the CNS, lipids are closely related to the formation and function of exosomes. Their dysregulation causes abnormalities in exosomes, which may, in turn, lead to dysfunctions in inter-neuronal communication and promote diseases. Therefore, the role of lipids in the treatment of neurological diseases through exosomes has received increasing attention. The aim of this review is to discuss the relationship between lipids and exosomes and their roles in CNS diseases.

Autism spectrum disorders (ASD) diagnostic procedure still lacks a uniform biological marker. This review gathers the information on microRNAs (miRNAs) specifically as a possible source of biomarkers of ASD. Extracellular vesicles, and their subset of exosomes, are believed to be a tool of cell-to-cell communication, and they are increasingly considered to be carriers of such a marker. The interest in studying miRNAs in extracellular vesicles grows in all fields of study and therefore should not be omitted in the field of neurodevelopmental disorders. The summary of miRNAs associated with brain cells and ASD either studied directly in the tissue or biofluids are gathered in this review. The heterogeneity in findings from different studies points out the fact that unified methods should be established, beginning with the determination of the accurate patient and control groups, through to sample collection, processing, and storage conditions. This review, based on the available literature, proposes the standardized approach to obtain the results that would not be affected by technical factors. Nowadays, the method of high-throughput sequencing seems to be the most optimal to analyze miRNAs. This should be followed by the uniformed bioinformatics procedure to avoid misvalidation. At the end, the proper validation of the obtained results is needed. With such an approach as is described in this review, it would be possible to obtain a reliable biomarker that would characterize the presence of ASD.

MicroRNAs (miRNAs) refer to a class of small endogenous non-coding RNAs that regulate gene expression at the post-transcriptional level. Emerging studies have shown that miRNAs play critical roles in tumorigenesis and cancer progression. However, roles and mechanisms of miRNA dysregulation in the pathogenesis of meningioma are not fully understood. Here, we first reviewed existing research of aberrantly expressed miRNAs identified by high throughput microarray profiling in meningioma. We also explored the potential of miRNA as biomarkers and therapeutic targets for novel treatment paradigms of meningiomas. In addition, we summarized recent researches that focused on the possible mechanisms involved in miRNA-mediate meningioma occurrence and progression. This review provides an overview of miRNA deregulation in meningioma and indicates the potential of miRNAs to be used as biomarkers or novel therapeutic targets.

Multiple sclerosis (MS) is a neurological disease characterized by neuroinflammation, demyelination and axonal degeneration along with loss of function in the central nervous system. For many years, research in MS has focused on the efficacy of pharmacological treatments. However, during the last years, many publications have been dedicated to the study of the efficacy of non-pharmacological strategies, such as physical exercise and cognitive training. Beneficial effects of the combination of both strategies on cognitive function have been described in both ageing adults and patients with neurodegenerative diseases, such as MS. The analysis of combining both physical and cognitive stimulation can be summarized by the environmental enrichment (EE) experiments, which are more suitable for animal models. EE refers to housing conditions consisting of exercise and cognitive and social stimulation. In this review, we will summarize the available studies that describe the influence of EE in both MS patients and MS animal models.

Encephalopathy related to Status Epilepticus during slow Sleep (ESES) is an age-dependent syndrome characterized by the appearance of neuropsychological and behavioral disorders associated with extreme activation of epileptic activity during sleep. The major goal of therapy in ESES is to prevent neuropsychological deficits. Effective therapy to reduce seizures and resolve the EEG pattern of status epilepticus during sleep (SES) may be crucial to improve long-term prognosis. However, whether to improve neurodevelopmental deficits by suppressing or eliminating SES remains unknown. The purpose of this article is to review current therapeutic options in ESES, in order to provide better alternatives. Treatment options consist of antiepileptic drugs, steroids, immunoglobulins, the ketogenic diet, and surgery. Maybe therapy targeted mechanisms can be developed with deep insight into the etiology of ESES.