A Dry EEG-System for Scientific Research and Brain–Computer Interfaces

Although it ranks among the oldest tools in neuroscientific research, electroencephalography (EEG) still forms the method of choice in a wide variety of clinical and research applications. In the context of brain–computer interfacing (BCI), EEG recently has become a tool to enhance human–machine interaction. EEG could be employed in a wider range of environments, especially for the use of BCI systems in a clinical context or at the homes of patients. However, the application of EEG in these contexts is impeded by the cumbersome preparation of the electrodes with conductive gel that is necessary to lower the impedance between electrodes and scalp. Dry electrodes could provide a solution to this barrier and allow for EEG applications outside the laboratory. In addition, dry electrodes may reduce the time needed for neurological exams in clinical practice. This study evaluates a prototype of a three-channel dry electrode EEG system, comparing it to state-of-the-art conventional EEG electrodes. Two experimental paradigms were used: first, event-related potentials (ERP) were investigated with a variant of the oddball paradigm. Second, features of the frequency domain were compared by a paradigm inducing occipital alpha. Furthermore, both paradigms were used to evaluate BCI classification accuracies of both EEG systems. Amplitude and temporal structure of ERPs as well as features in the frequency domain did not differ significantly between the EEG systems. BCI classification accuracies were equally high in both systems when the frequency domain was considered. With respect to the oddball classification accuracy, there were slight differences between the wet and dry electrode systems. We conclude that the tested dry electrodes were capable to detect EEG signals with good quality and that these signals can be used for research or BCI applications. Easy to handle electrodes may help to foster the use of EEG among a wider range of potential users

Lipocalin-2 is involved in emotional behaviors and cognitive function

Lipocalin-2 is involved in emotional behaviors and cognitive functionLipocalin-2 (LCN2), an iron-related protein well described to participate in the innate immune response, has been shown to modulate spine morphology and to regulate neuronal excitability. In accordance, LCN2-null mice are reported to have stress-induced anxiety. Here we show that, under standard housing conditions, LCN2-null mice display anxious and depressive-like behaviors, as well as cognitive impairment in spatial learning tasks. These behavioral alterations were associated with a hyperactivation of the hypothalamic-pituitary-adrenal axis and with an altered brain cytoarchitecture in the hippocampus. More specifically, we found that the granular and pyramidal neurons of the ventral hippocampus, a region described to be associated with emotion, were hypertrophic, while neurons from the dorsal hippocampus, a region implicated in memory and cognition, were atrophic. In addition, LCN2-null mice presented synaptic impairment in hippocampal long-term potentiation. Whether the LCN2 effects are mediated through modulation of the level of corticosteroids or through a novel mechanism, the present observations bring further into light this immune-related protein as a player in the fine-tuning of behavior and of synaptic activity.We are grateful to Professor Shizuo Akira and Professor Cevayir Coban for the LCN2-null mice in the BALB/c background and to Professor Trude Flo for the LCN2-null mice in C57BL/6J background. Ana C. Ferreira, Sandro D. Mesquita, and Ashley Novais are recipients of Ph.D. and Fernanda Marques and Vitor Pinto are recipients of postdoctoral fellowships from Fundacao para a Ciencia e Tecnologia (Portugal)

Lipocalin 2 is present in the EAE brain and is modulated by natalizumab

The authors acknowledge the BiogenIdec, for providing Natalizumab (BiogenIdec, Boston, MA, USA). We are thankful to theCOST(European Cooperation in Science and Technology) Action NEURINFNETBM0603. We also thank Dr. Nadine Santos for critically reviewing this manuscript.Multiple sclerosis (MS) is a demyelinating disease that causes major neurological disability in young adults. A definitive diagnosis at the time of the first episode is still lacking, but since early treatment leads to better prognosis, the search for early biomarkers is needed. Here we characterized the transcriptome of the choroid plexus (CP), which is part of the blood-brain barriers (BBBs) and the major site of cerebrospinal fluid production, in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS. In addition, cerebrospinal fluid samples from two cohorts of patients with MS and with optic neuritis (ON) were analyzed to confirm the clinical relevance of the findings. Genes encoding for adhesion molecules, chemokines and cytokines displayed the most altered expression, supporting the role of CP as a site of immune-brain interaction in MS. The gene encoding for lipocalin 2 was the most up-regulated; notably, the cerebrospinal fluid lipocalin 2 levels coincided with the active phases of the disease. Immunostaining revealed that neutrophils infiltrating the CP were the source of the increased lipocalin 2 expression in this structure. However, within the brain, lipocalin 2 was also detected in astrocytes, particularly in regions typically affected in patients with MS. The increase of lipocalin 2 in the cerebrospinal fluid and in astrocytes was reverted by natalizumab treatment. Most importantly, the results obtained in the murine model were translatable into humans since patients from two different cohorts presented increased cerebrospinal fluid lipocalin 2 levels. The findings support lipocalin 2 as a valuable molecule for the diagnostic/monitoring panel of MS.This work was supported by a grant from The Dana Foundation (USA) and by a grant from Fundação para a Ciência e Tecnologia(FCT, Portugal) (PIC/IC/83231/2007). Fernanda Marques and Sandro D. Mesquita are recipients of postdoctoral and doctoral fellow- ships from FCT, Portugal, respectively

Modulation of iron metabolism in aging and in Alzheimer’s disease: relevance of the choroid plexus.

Iron is essential for mammalian cellular homeostasis. However, in excess, it promotes free radical formation and is associated with aging-related progressive deterioration and with neurodegenerative disorders such as Alzheimer’s disease (AD). There are no mechanisms to excrete iron, which makes iron homeostasis a very tightly regulated process at the level of the intestinal absorption. Iron is believed to reach the brain through receptor mediated endocytosis of iron-bound transferrin by the brain barriers, the blood-cerebrospinal (CSF) fluid barrier, formed by the choroid plexus (CP) epithelial cells and the blood-brain barrier formed by the endothelial cells of the brain capillaries. Importantly, the CP epithelial cells are responsible for producing most of the CSF, the fluid that fills the brain ventricles and the subarachnoid space. Recently, the finding that the CP epithelial cells display all the machinery to locally control iron delivery into the CSF may suggest that the general and progressive senescence of the CP may be at the basis of the impairment of regional iron metabolism, iron-mediated toxicity and the increase in inflammation and oxidative stress that occurs with aging and, particularly, in AD