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Cerebral venous thrombosis (CVT), although accounting for only 0.5-1% of all strokes, remains a potentially fatal neurological emergency, which must be promptly diagnosed and treated. Consisting of two parts, this review aims to highlight the most important data from recent years regarding diagnosis and treatment of CVT, illustrating both the current modern therapeutic approach and the future research directions in the field. Regarding the clinical diagnosis, the neurologist may sometimes have difficulties in recognizing this pathology, given the diverse clinical picture of the acute stage of CVT that can mimic various neurological disorders. In addition, although most risk factors (procoagulation status, infections, trauma, systemic diseases) are known and can be easily detected, in a significant percentage of cases the etiology remains uncertain. For paraclinical diagnosis, among the imaging investigations essential to support the diagnosis, CT angiography and MRI venography are reliable alternatives to digital subtraction angiography which represent the gold standard nowadays. In terms of treatment, international guidelines provide general directions for anticoagulation, with low molecular weight heparin being highly recommended. Regarding invasive treatment methods (thrombolysis, thrombectomy) that could be used in severe cases where anticoagulation has been shown to be insufficient, as well as symptomatic therapy, the evidence is often insufficient, new randomized clinical trials with large cohorts of patients being required.

Nowadays, the success of multiple sclerosis therapy does not only mean the absence of relapses or the existence of a stationary clinical status under disease-modifying therapy, but the maintenance of a high quality of life index. Thus, in recent years, the attention of neurologists has focused on the relationship between depression and MS, depression being the most important factor influencing the MS patient’s quality of life. In this regard, the article aims to present a selection of the most important scientific data published during the last 5 years on this topic. Structured in two parts, the initial issue discussed is the etiopathogenesis of depression in MS, with focus on the presentation of theories on the causes of depressive symptoms in demyelinating disease, as well as the intricate relationship between the two clinical entities. Subsequently, the article focuses on capturing the latest developments in currently available pharmacological and non-pharmacological therapeutic means and future prospects for treatment.

Sleep-wake disorders play an important role among non-motor symptoms in Parkinson’s Disease, being a constant subject of research in recent years. There are a multitude of sleep-wake disturbances that worsen the patient’s quality of life, insomnia and excessive daytime sleepiness being two of the most frequent complaints. The aim of this review is to highlight the most relevant clinical trials conducted during the last 5 years, focusing on the problematic of insomnia and daytime sleepiness correlated with Parkinson’s Disease and its treatment. Three electronic databases (Pubmed, Science Direct and Google Scholar) were searched during March and April 2020 for articles on this topic, finally selecting 21 most relevant articles that we have included in this review. Interesting aspects regarding correlation between sleep-wake disorders and Parkinson’s disease were found, showing that non-motor symptoms may be independent of the disease itself. We discussed the most recent advances in treatment opportunities and the adverse effects, with insomnia and daytime sleepiness among the most common complaints. Besides newly developed pharmacological therapy, consisting in mostly dopaminergic agonists or levodopa adjuvant drugs. Other possibly effective therapies on sleep-wake disorders such as deep brain stimulation, dietary changes, bright light therapy and alternative medicine protocols are also reviewed. Insomnia and excessive daytime sleepiness are common complaints in Parkinson’s disease patients, being either self-standing non-motor symptoms or adverse effects of the antiparkinsonian medication, diminishing patient’s quality of life. The effervescence of research on this topic shows promising results, with new clinical trials still to come in the near future.

Background: Parkinson’s disease (PD) remains a challenge for neurologists, particularly in its advanced stages when non-motor symptoms become a burden for the patient. While motor symptoms may be satisfactorily controlled with levodopa therapy or continuous levodopa/carbidopa intestinal gel (LCIG) administration, autonomic, sleep and mental disorders are hard to treat. During the last years, researchers have shifted their interest more to non-motor symptoms, PD being now considered a complex multiorgan impairment. Objective: The aim of this study was to describe non-motor symptoms in 40 Romanian patients diagnosed with PD, under conventional and LCIG administration treatment. Methods: A cross-sectional observational study was conducted, consisting of two groups of 20 patients each: the first group comprised PD patients who received conventional Levodopa treatment, while the second group was formed of patients receiving LCIG therapy. Various data concerning patient’s age, gender, duration of illness, comorbidities, motor and non-motor symptoms were recorded. The data were processed in SPSS v.20. Results: Subjects under continuous LCIG administration, although showing amelioration of motor symptoms, complained more frequently of constipation, mental, and sleeping disorders (statistically significant). Regarding anosmia, orthostatic hypotension, hypersalivation, urinary incontinence and restless legs syndrome, no statistical significant difference was observed between the two groups (p > 0.05). Conclusion: Nowadays, more research is conducted on non-motor symptoms in PD patients, as therapeutic measures try to limit these burdens, in order to improve patient’s quality of life.

Despite the significant impact of Alzheimer’s disease (AD) at individual and socioeconomic levels and the numerous research studies carried out on this topic over the last decades, the treatments available in daily clinical practice remain less than satisfactory. Among the accepted etiopathogenic hypotheses, the amyloidogenic pathway theory, although intensively studied and even sometimes controversial, is still providing relevant theoretical elements for understanding the etiology of AD and for the further development of possible therapeutic tools. In this sense, this review aims to offer new insights related to beta amyloid (Aβ), an essential biomarker in AD. First the structure and function of Aβ in normal and pathological conditions are presented in detail, followed by a discussion on the dynamics of Aβ at the level of different biological compartments. There is focus on Aβ elimination modalities at central nervous system (CNS) level, and clearance via the blood–brain barrier seems to play a crucial/dominant role. Finally, different theoretical and already-applied therapeutic approaches for CNS Aβ elimination are presented, including the recent “peripheral sink therapeutic strategy” and “cerebrospinal fluid sinks therapeutic strategy”. These data outline the need for a multidisciplinary approach designed to deliver a solution to stimulate Aβ clearance in more direct ways, including from the cerebrospinal fluid level.

Here, we reported a study on the detection and electrical characterization of both cancer cell line and primary tumor cells. Dielectrophoresis (DEP) and electrical impedance spectroscopy (EIS) were jointly employed to enable the rapid and label-free differentiation of various cancer cells from normal ones. The primary tumor cells that were collected from two colorectal cancer patients, cancer cell lines (SW-403, Jurkat, and THP-1), and healthy peripheral blood mononuclear cells (PBMCs) were trapped first at the level of interdigitated microelectrodes with the help of dielectrophoresis. Correlation of the cells dielectric characteristics that was obtained via electrical impedance spectroscopy (EIS) allowed evident differentiation of the various types of cell. The differentiations were assigned to a “dielectric phenotype” based on their crossover frequencies. Finally, Randles equivalent circuit model was employed for highlighting the differences with regard to a series group of charge transport resistance and constant phase element for cancerous and normal cells.

Background: Given the common elements in the pathophysiological theories that try to explain the appearance and evolution of obesity and multiple sclerosis, the association between the two pathologies has become an increasingly researched topic in recent years. On the one hand, there is the chronic demyelinating inflammation caused by the autoimmune cascade of multiple sclerosis, while on the other hand, according to the latest research, it has been shown that obesity shares an inflammatory component with most chronic diseases. Methods: The authors performed independent research of the available literature in the most important electronic databases (PubMed, Google Scholar, Embase, and Science Direct) in February 2021. After applying the exclusion criteria, the reviewers focused on the most relevant articles published during the last 10 years with respect to epidemiology and pathophysiology. Results: The data presented are a step forward in trying to elucidate the intricate relationship between obesity and MS, especially the causal relationship between childhood and adolescent obesity and MS, focusing on the epidemiological associations observed in the most relevant observational studies conducted in recent years. In the second part, the authors comment on the latest findings related to the pathophysiological mechanisms that may explain the correlations between obesity and multiple sclerosis, focusing also on the role of adipokines. Conclusions: Based on available epidemiological data, obesity in early life appears to be strongly associated with a higher risk of MS development, independent of other risk factors. Although much research has been done on the pathophysiology of obesity, MS, their possible common mechanism, and the role of adipokines, further studies are needed in order to explain what remains unknown. No relevant data were found regarding the association between obesity, disability (high EDSS score), and mortality risk in MS patients. Thus, we consider that this topic should be elucidated in future research.

Neoplasia occurs as a result of genetic mutations. Research evaluating the association between gene mutations and skin cancer is limited and has produced inconsistent results. There are no established guidelines for screening skin cancer at molecular level. It should also be noted that the combinations of some mutations may play a role in skin tumors’ biology and immune response. There are three major types of skin cancer, and the originality of this study comes from its approach of each of them.