Functional Neuroanatomy of the Normal and Pathological Basal Ganglia.

The term "basal ganglia" refers to a group of interconnected subcortical nuclei engaged in motor planning and movement initiation, executive functions, behaviors, and emotions. Dopamine released from the substantia nigra is the underlying driving force keeping the basal ganglia network under proper equilibrium and, indeed, reduction of dopamine levels triggers basal ganglia dysfunction, setting the groundwork for several movement disorders. The canonical basal ganglia model has been instrumental for most of our current understanding of the normal and pathological functioning of this subcortical network.

Applying the IEEE BRAIN neuroethics framework to intra-cortical brain-computer interfaces.

. Brain-computer interfaces (BCIs) are neuroprosthetic devices that allow for direct interaction between brains and machines. These types of neurotechnologies have recently experienced a strong drive in research and development, given, in part, that they promise to restore motor and communication abilities in individuals experiencing severe paralysis.

Translation and cross-cultural adaptation of 14-item Mediterranean Diet Adherence Screener and low-fat diet adherence questionnaire.

Background And Aims: The Mediterranean diet and the low-fat diet are recognized as cardioprotective dietary patterns, and the use of validated instruments that quickly identify adherence to these diets is very useful in the daily practice of the nutritionist. Our aim was to translate and cross-culturally adapt the 14-point Mediterranean Diet Adherence Screener (MEDAS) and a 9-item quantitative score of compliance with the low-fat diet (low-fat diet questionnaire) to the Brazilian Portuguese language.

Methods: The process of translation and cultural adaptation was conducted in six stages: initial translation, synthesis of translations, back-translation, proof of cross-cultural equivalence, pre-final version testing, and final evaluation of the cultural adaptation process.

RNAi-Based GluN3A Silencing Prevents and Reverses Disease Phenotypes Induced by Mutant huntingtin.

Huntington's disease (HD) is a dominantly inherited neurodegenerative disease caused by expansion of a polyglutamine tract in the huntingtin protein. HD symptoms include severe motor, cognitive, and psychiatric impairments that result from dysfunction and later degeneration of medium-sized spiny neurons (MSNs) in the striatum. A key early pathogenic mechanism is dysregulated synaptic transmission due to enhanced surface expression of juvenile NMDA-type glutamate receptors containing GluN3A subunits, which trigger the aberrant pruning of synapses formed by cortical afferents onto MSNs.

Self-perceived level of competitiveness, tension, and dependency and lifestyles in the 'Seguimiento Universidad de Navarra' cohort study.

Objective: The objective of this study is to assess the differences in lifestyles according to levels of self-perceived competitiveness, psychological tension, and dependency in a Mediterranean cohort of university graduates.

Study Design: Levels of personality traits, food consumption, nutrient intake, eating attitudes, physical activity, sedentary lifestyle, and alcohol and tobacco consumption were assessed through a questionnaire administered at baseline. This was a cross-sectional study in the context of the Seguimiento Universidad de Navarra cohort.

Metabolic Predictors of Incident Coronary Heart Disease in Women.

Background: Although metabolomic profiling offers promise for the prediction of coronary heart disease (CHD), and metabolic risk factors are more strongly associated with CHD in women than men, limited data are available for women.

Methods: We applied a liquid chromatography-tandem mass spectrometry metabolomics platform to measure 371 metabolites in a discovery set of postmenopausal women (472 incident CHD cases, 472 controls) with validation in an independent set of postmenopausal women (312 incident CHD cases, 315 controls).

Results: Eight metabolites, primarily oxidized lipids, were significantly dysregulated in cases after the adjustment for matching and CHD risk factors in both the discovery and validation data sets.

The Role of Diet in the Pathogenesis of Cholesterol Gallstones.

Cholesterol gallstone disease is a major health problem in Westernized countries and depends on a complex interplay between genetic factors, lifestyle and diet, acting on specific pathogenic mechanisms. Overweigh, obesity, dyslipidemia, insulin resistance and altered cholesterol homeostasis have been linked to increased gallstone occurrence, and several studies point to a number of specific nutrients as risk- or protective factors with respect to gallstone formation in humans. There is a rising interest in the identification of common and modifiable dietetic factors that put the patients at risk of gallstones or that are able to prevent gallstone formation and growth.

Chromium Exposure and Risk of Cardiovascular Disease in High Cardiovascular Risk Subjects - Nested Case-Control Study in the Prevention With Mediterranean Diet (PREDIMED) Study.

Background: Epidemiological data on chromium (Cr) exposure and the risk of cardiovascular disease (CVD) are still limited. Toenail Cr level (TCL) provides a time-integrated measure reflecting long-term Cr exposure. We measured TCL to assess the hypothesis that long-term Cr exposure was inversely associated with incident CVD in a population at high risk for CVD.

Emerging roles of GluN3-containing NMDA receptors in the CNS.

GluN3-containing NMDA receptors (GluN3-NMDARs) are rarer than the 'classical' NMDARs, which are composed solely of GluN1 and GluN2 subunits, and have non-conventional biophysical, trafficking and signalling properties. In the CNS, they seem to have important roles in delaying synapse maturation until the arrival of sensory experience and in targeting non-used synapses for pruning. The reactivation of GluN3A expression at inappropriate ages may underlie maladaptive synaptic rearrangements observed in addiction, neurodegenerative diseases and other major brain disorders.

Adenovirus expressing β2-microglobulin recovers HLA class I expression and antitumor immunity by increasing T-cell recognition.

Optimal tumor cell surface expression of human leukocyte antigen (HLA) class I molecules is essential for the presentation of tumor-associated peptides to T-lymphocytes. However, a hallmark of many types of tumor is the loss or downregulation of HLA class I expression associated with ineffective tumor antigen presentation to T cells. Frequently, HLA loss can be caused by structural alterations in genes coding for HLA class I complex, including the light chain of the complex, β2-microglobulin (β2m).

Normal neurological outcome after congenital thyrotoxicosis: prognostic value of observation of general movements.

We followed up a patient born preterm with congenital thyrotoxicosis by observing her general movements (GMs) in accordance with Prechtl's method. Initially a chaotic pattern was observed. Along with the normalization of thyroid hormones, the GM pattern changed to a poor repertoire at four weeks of life, full-blown writhing movements at six weeks and fidgety movements at the age of four months.

Language impairment: stepwise or slowly progressive?

MRI showed ischemic lesions of the left hemisphere in a patient with a worsening language disturbance that by history could be caused either by ischemia or by a focal degenerative brain disorder. A positron emission tomography study indicated the presence of a degenerative disorder, the most common cause of which is tau-positive pathology.

Increased oxidative damage to DNA in an animal model of amyotrophic lateral sclerosis.

Substantial evidence suggest that oxidative damage may play a role in the pathogenesis of Amyotrophic Lateral Sclerosis (ALS). We examined levels of 8-Hydroxy-2'-deoxyguanosine (8OH2'dG) in the nuclear DNA from the spinal cord, frontal cortex, striatum and cerebellum from G93A mice at 60, 90, and 120 days of age. We also used in vivo microdialysis to measure free levels of 8OH2'dG and 8-Hydroxyguanine (8OHG) at the same time points in the frontal cortex of G93A mice.

Homeostatic plasticity and NMDA receptor trafficking.

Learning, memory and brain development are associated with long-lasting modifications of synapses that are guided by specific patterns of neuronal activity. Such modifications include classical Hebbian plasticities (such as long-term potentiation and long-term depression), which are rapid and synapse-specific, and others, such as synaptic scaling and metaplasticity, that work over longer timescales and are crucial for maintaining and orchestrating neuronal network function. The cellular mechanisms underlying Hebbian plasticity have been well studied and involve rapid changes in the trafficking of highly mobile AMPA receptors.

Incidence of eating disorders in Navarra (Spain).

Purpose: To estimate the overall annual incidence and age group distribution of eating disorders in a representative sample of adolescent female residents of Navarra, Spain.

Methods: We studied a representative sample of 2734 adolescent Navarran females between 13 and 22 years of age who were free of any eating disorder at the start of our study. Eighteen months into the study, we visited the established centers and the eating attitudes test (EAT-40) and eating disorder inventory (EDI) Questionnaires were administered to the entire study population.

Strong mixed-handedness in schizophrenia.

There is still considerable discussion of whether schizophrenia is a lateralized brain disorder. In fact, schizophrenic patients appear to exhibit a shift away from dexterity, as confirmed by the majority of the 23 publications dealing with this question (14 positive, seven null, two paradoxical). However, quite a few of these positive studies have distinguished between left-handedness and mixed-handedness (MH), thus lacking specificity.

Antidepressant-like activity of VN2222, a serotonin reuptake inhibitor with high affinity at 5-HT1A receptors.

It has been suggested that drugs combining serotonin (5-hydroxytryptamine, 5-HT) transporter blockade and 5-HT1A autoreceptor antagonism could be a novel strategy for a shorter onset of action and higher therapeutic efficacy of antidepressants. The present study was aimed at characterizing the pharmacology of 1-(3-benzo[b]tiophenyl)-3-[4-(2-methoxyphenyl)-1-piperazinyl]-1-propanol (VN2222) a new synthetic compound with high affinity at both the 5-HT transporter and 5-HT1A receptors and devoid of high affinity at other receptors studied, with the only exception of alpha1-adrenoceptors. In keeping with the binding affinity at the 5-HT transporter, VN2222 inhibited 5-HT uptake in vitro both in rat cortical synaptosomes and in mesencephalic cultures and also in vivo when administered locally into the rat ventral hippocampus.

Serotonin 5-HT(1A) receptor expression is selectively enhanced in the striosomal compartment of chronic parkinsonian monkeys.

Cynomolgus monkeys (Macaca fascicularis) were chronically treated with the dopaminergic neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) until stable parkinsonism was reached. Two months later, monkeys were sacrificed and monoamine content was measured in different brain regions of the lesioned monkeys and of age-matched controls. 5-HT(1A) serotonin receptor density was measured in coronal sections labeled with [(3)H]8-OH-DPAT.

2-Deoxy-D-glucose prevents and nicotinamide potentiates 3, 4-methylenedioxymethamphetamine-induced serotonin neurotoxicity.

Neurotoxicity induced by different substituted amphetamines has been associated with the exhaustion of intracellular energy stores. Accordingly, we examined the influence of 2-deoxy-D-glucose (2-DG), a competitive inhibitor of glucose uptake and metabolism, and nicotinamide, an agent that improves energy metabolism, on 3, 4-methylenedioxymethamphetamine (MDMA)-induced 5-hydroxytryptamine (5-HT; serotonin) deficits. Administration of MDMA (15 mg/kg i.

Effect of p-chloroamphetamine on 5-HT1A and 5-HT7 serotonin receptor expression in rat brain.

The aim of this study was to investigate if p-chloroamphetamine (PCA), which is neurotoxic to serotonin (5-HT) nerve terminals, was able to induce, like 3,4-methylenedioxymethamphetamine, a region-specific regulation of 5-HT1A receptor mRNA expression. The effect of PCA on the expression of 5-HT7 receptors, which share some pharmacological properties with 5-HT1A receptors, was comparatively studied. PCA (2 x 5 mg/kg) produced a lasting depletion of 5-HT content in the rat frontal cortex and hippocampus.

Implanted BDNF-producing fibroblasts prevent neurotoxin-induced serotonergic denervation in the rat striatum.

Degeneration of serotonergic fibers in the rat striatum was produced by local administration of the serotonergic neurotoxin 5, 7-dihydroxytryptamine (5,7-DHT) or the dopaminergic neurotoxin 1-methyl-4-phenylpyridinium (MPP(+)), which is also toxic to serotonergic neurons. One week before neurotoxin administration, fibroblasts engineered to express the human BDNF gene were grafted into the mesencephalon, dorsal to the substantia nigra. Rats implanted with fibroblasts expressing the LacZ gene were used as controls, as well as sham-operated animals (not injected with any neurotoxin).

Anxiogenic-like effects and reduced stereological counting of immunolabelled 5-hydroxytryptamine6 receptors in rat nucleus accumbens by antisense oligonucleotides.

The physiological role of 5-hydroxytryptamine6 receptors in the central nervous system has not yet been elucidated. The high affinity of various psychotropic drugs for 5-hydroxytryptamine6 receptors has led to the suggestion that this receptor type may be a novel target in neuropsychiatry. We have found that continuous intracerebroventricular administration of a 5-hydroxytryptamine6 receptor antisense oligonucleotide, but not of a missense oligonucleotide, produced an anxiogenic-like response in rats using two different models of anxiety, the social interaction test and the elevated plus-maze.