Effects of Exercise on Physical and Mental Health, and Cognitive and Brain Functions in Schizophrenia: Clinical and Experimental Evidence

Exercise promotes several health benefits, such as cardiovascular, musculoskeletal and cardiorespiratory improvements. It is believed that the practice of exercise in individuals with psychiatric disorders, e.g. schizophrenia, can cause significant changes. Schizophrenic patients have problematic lifestyle habits compared with general population; this may cause a high mortality rate, mainly caused by cardiovascular and metabolic diseases. Thus, the aim of this study is to investigate changes in physical and mental health, cognitive and brain functioning due to the practice of exercise in patients with schizophrenia. Although still little is known about the benefits of exercise on mental health, cognitive and brain functioning of schizophrenic patients, exercise training has been shown to be a beneficial intervention in the control and reduction of disease severity. Type of training, form of execution, duration and intensity need to be better studied as the effects on physical and mental health, cognition and brain activity depend exclusively of interconnected factors, such as the combination of exercise and medication. However, one should understand that exercise is not only an effective nondrug alternative, but also acts as a supporting linking up interventions to promote improvements in process performance optimization. In general, the positive effects on mental health, cognition and brain activity as a result of an exercise program are quite evident. Few studies have been published correlating effects of exercise in patients with schizophrenia, but there is increasing evidence that positive and negative symptoms can be improved. Therefore, it is important that further studies be undertaken to expand the knowledge of physical exercise on mental health in people with schizophrenia, as well as its dose-response and the most effective type of exercise.

Potenciais evocados auditivos de média latência em adultos com epilepsia

Introdução Os potenciais evocados auditivos de média latência (PEAML) reflectem actividade neuronal mesencefáfica, mais precisamente da região tálamo-cortical, dos colículos inferiores e da formação reticular. A epilepsia é caracterizada por variadas manifestações anormais do comportamento cerebral, sendo descrita como uma perturbação da função cerebral, tendo origem numa descarga anómala de um conjunto ou da totalidade dos neurónios do córtice cerebral. Está documentado, que as descargas eléctricas provocadas pelas crises de epilepsia podem levar a perdas neuronais, pelo que poderão existir alterações nos PEAML. Objectivos A escassa existência de literatura sobre o tema e a não investigação na população portuguesa, originou a execução deste estudo, que teve como objectivo investigar e documentar a existência de alterações ou achados nos componentes neuronais de média latência (PEAML), numa amostra de portugueses com epilepsia. Metodologia Foram realizados PEAML a um grupo de controlo (GC) composto por 16 participantes e a um grupo clínico (GCL) de 8 participantes com epilepsia, sendo analisados os componentes Na, Pa e Na-Pa quanto à sua morfologia, latência e amplitude. Resultados A morfologia das ondas e a presença de epilepsia não estão associados, no entanto, contrariamente ao GC que evidenciou latências e amplitudes de Na, Pa e Na-Pa dentro dos padrões de normalidade, a alteração ou ausência de respostas por parte do GCL é significativa na totalidade das medidas investigadas. Conclusão Em epilepsias generalizadas e focais do lobo temporal os PEAML evidenciam alterações, tal achado poderá ser eventualmente justificado pela propagação ascendente e descendente da informação auditiva se encontrar comprometida, devido a sequelas deixadas pelas crises epilépticas nas vias auditivas mesencefálicas. As alterações verificadas foram uma morfologia anómala das ondas ou ausência das mesmas.

Uso de Interfaces Cérebro-computador na comunicação de pessoas com Síndrome de Encarceramento

Os avanços nas Interfaces Cérebro-máquina, resultantes dos avanços no tratamento de sinal e da inteligência artificial, estão a permitir-nos aceder à atividade cerebral, descodificá-la, e usála para comandar dispositivos, sejam eles braços artificiais ou computadores. Isto é muito mais importante quando os utilizadores são pessoas que perderam a capacidade de comunicar, embora mantenham as suas capacidades cognitivas intactas. O caso mais extremo desta situação é o das pessoas afetadas pela Síndrome de Encarceramento. Este trabalho pretende contribuir para a melhoria da qualidade de vida das pessoas afetadas por esta síndrome, disponibilizando-lhes um meio de comunicação adaptado às suas limitações. É essencialmente um estudo de usabilidade aplicada a um tipo de utilizador extremamente diminuído na sua capacidade de interação. Nesta investigação começamos por compreender a Síndrome de Encarceramento e as limitações e capacidades das pessoas afetadas por ela. Abordamos a neuroplasticidade, o que é, e em que medida é importante para a utilização das Interfaces Cérebro-máquina. Analisamos o funcionamento destas interfaces, e os fundamentos científicos que o suportam. Finalmente, com todo este conhecimento em mãos, investigamos e desenvolvemos métodos que nos permitissem otimizar as limitadas capacidades do utilizador na sua interação com o sistema, minimizando o esforço e maximizando o desempenho. Foi para o efeito desenhado e implementado um protótipo que nos permitisse validar as soluções encontradas.

Effects of early life permethrin exposure on spatial working memory and on monoamine levels in different brain areas of pre-senescent rats

Pesticide exposure during brain development could represent an important risk factor for the onset of neurodegenerative diseases. Previous studies investigated the effect of permethrin (PERM) administered at 34 mg/kg, a dose close to the no observable adverse effect level (NOAEL) from post natal day (PND) 6 to PND 21 in rats. Despite the PERM dose did not elicited overt signs of toxicity (i.e. normal body weight gain curve), it was able to induce striatal neurodegeneration (dopamine and Nurr1 reduction, and lipid peroxidation increase). The present study was designed to characterize the cognitive deficits in the current animal model. When during late adulthood PERM treated rats were tested for spatial working memory performances in a T-maze-rewarded alternation task they took longer to choose for the correct arm in comparison to age matched controls. No differences between groups were found in anxiety-like state, locomotor activity, feeding behavior and spatial orientation task. Our findings showing a selective effect of PERM treatment on the T-maze task point to an involvement of frontal cortico-striatal circuitry rather than to a role for the hippocampus. The predominant disturbances concern the dopamine (DA) depletion in the striatum and, the serotonin (5-HT) and noradrenaline (NE) unbalance together with a hypometabolic state in the medial prefrontal cortex area. In the hippocampus, an increase of NE and a decrease of DA were observed in PERM treated rats as compared to controls. The concentration of the most representative marker for pyrethroid exposure (3-phenoxybenzoic acid) measured in the urine of rodents 12 h after the last treatment was 41.50 µ/L and it was completely eliminated after 96 h.

Acetyl-L-Carnitine Prevents Methamphetamine-Induced Structural Damage on Endothelial Cells via ILK-Related MMP-9 Activity

Methamphetamine (METH) is a potent psychostimulant highly used worldwide. Recent studies evidenced the involvement of METH in the breakdown of the blood-brain-barrier (BBB) integrity leading to compromised function. The involvement of the matrix metalloproteinases (MMPs) in the degradation of the neurovascular matrix components and tight junctions (TJs) is one of the most recent findings in METH-induced toxicity. As BBB dysfunction is a pathological feature of many neurological conditions, unveiling new protective agents in this field is of major relevance. AcetylL-carnitine (ALC) has been described to protect the BBB function in different paradigms, but the mechanisms underling its action remain mostly unknown. Here, the immortalized bEnd.3 cell line was used to evaluate the neuroprotective features of ALC in METH-induced damage. Cells were exposed to ranging concentrations of METH, and the protective effect of ALC 1 mM was assessed 24 h after treatment. F-actin rearrangement, TJ expression and distribution, and MMPs activity were evaluated. Integrin-linked kinase (ILK) knockdown cells were used to assess role of ALC in ILK mediated METHtriggered MMPs’ activity. Our results show that METH led to disruption of the actin filaments concomitant with claudin-5 translocation to the cytoplasm. These events were mediated by MMP-9 activation in association with ILK overexpression. Pretreatment with ALC prevented METH-induced activation of MMP-9, preserving claudin-5 location and the structural arrangement of the actin filaments. The present results support the potential of ALC in preserving BBB integrity, highlighting ILK as a new target for the ALC therapeutic use.

Activity-Dependent Neurorehabilitation Beyond Physical Trainings: "Mental Exercise" Through Mirror Neuron Activation

The activity dependent brain repair mechanism has been widely adopted in many types of neurorehabilitation. The activity leads to target specific and non-specific beneficial effects in different brain regions, such as the releasing of neurotrophic factors, modulation of the cytokines and generation of new neurons in adult hood. However physical exercise program clinically are limited to some of the patients with preserved motor functions; while many patients suffered from paralysis cannot make such efforts. Here the authors proposed the employment of mirror neurons system in promoting brain rehabilitation by "observation based stimulation". Mirror neuron system has been considered as an important basis for action understanding and learning by mimicking others. During the action observation, mirror neuron system mediated the direct activation of the same group of motor neurons that are responsible for the observed action. The effect is clear, direct, specific and evolutionarily conserved. Moreover, recent evidences hinted for the beneficial effects on stroke patients after mirror neuron system activation therapy. Finally some music-relevant therapies were proposed to be related with mirror neuron system.