Narcolepsy patients have antibodies that stain distinct cell populations in rat brain and influence sleep patterns.

Narcolepsy is a chronic sleep disorder, likely with an autoimmune component. During 2009 and 2010, a link between A(H1N1)pdm09 Pandemrix vaccination and onset of narcolepsy was suggested in Scandinavia. In this study, we searched for autoantibodies related to narcolepsy using a neuroanatomical array: rat brain sections were processed for immunohistochemistry/double labeling using patient sera/cerebrospinal fluid as primary antibodies. Sera from 89 narcoleptic patients, 52 patients with other sleep-related disorders (OSRDs), and 137 healthy controls were examined. Three distinct patterns of immunoreactivity were of particular interest: pattern A, hypothalamic melanin-concentrating hormone and proopiomelanocortin but not hypocretin/orexin neurons; pattern B, GABAergic cortical interneurons; and pattern C, mainly globus pallidus neurons. Altogether, 24 of 89 (27%) narcoleptics exhibited pattern A or B or C. None of the patterns were exclusive for narcolepsy but were also detected in the OSRD group at significantly lower numbers. Also, some healthy controls exhibited these patterns. The antigen of pattern A autoantibodies was identified as the common C-terminal epitope of neuropeptide glutamic acid-isoleucine/alpha-melanocyte-stimulating hormone (NEI/alphaMSH) peptides. Passive transfer experiments on rat showed significant effects of pattern A human IgGs on rapid eye movement and slow-wave sleep time parameters in the inactive phase and EEG theta-power in the active phase. We suggest that NEI/alphaMSH autoantibodies may interfere with the fine regulation of sleep, contributing to the complex pathogenesis of narcolepsy and OSRDs. Also, patterns B and C are potentially interesting, because recent data suggest a relevance of those brain regions/neuron populations in the regulation of sleep/arousal

Self-reassurance, not self-esteem, serves as a buffer between self-criticism and depressive symptoms

Several studies suggest that self‐criticism and self‐reassurance operate through different mechanisms and might interact with each other. This study examined the hypothesis that self‐reassurance serves as a buffer between self‐criticism and depressive symptoms in a way that self‐esteem, which is rooted in a different motivational system, may not. We hypothesized that self‐criticism would be correlated with high levels of depressive symptoms but that this association would be weaker at higher levels of self‐reassurance abilities. We also hypothesized that self‐esteem, a self‐relating process based on feeling able and competent to achieve life goals, would not buffer the relationship between self‐criticism and depression. Self‐criticism, self‐reassurance, depressive symptoms, and self‐esteem were assessed in a sample of 419 participants (66% females; Mage = 33.40, SD = 11.13). At higher levels of self‐reassurance, the relationship between self‐criticism and depressive symptoms became non‐significant, supporting the buffering hypothesis of self‐reassurance. Despite the high correlation between self‐esteem and self‐reassurance, self‐esteem did not moderate the relationship between self‐criticism and depressive symptoms. Results support the growing evidence that not all positive self‐relating processes exert the same protective function against psychopathological consequences of self‐criticism. Implications for psychotherapy and the validity of using compassion‐focused interventions with clients with self‐critical issues are discussed. Self‐reassurance and self‐criticism are distinct processes and they should not be considered positive and negative variations of a single dimension. Different types of positive self‐relating do not show the same correlation with depressive symptoms. The ability to be self‐reassuring protects against the psychopathological correlates of self‐criticism while having high self‐esteem does not. Compassion‐focused interventions are promising avenues to help clients counteract the negative impact of self‐criticism on mood.N/

Why do the poor save so little?

SIGLEAvailable from British Library Document Supply Centre-DSC:3553.800(98-20) / BLDSC - British Library Document Supply CentreGBUnited Kingdo

Reward, emotion and consumer choice: from neuroeconomics to neurophilosophy

Neuroeconomics has found no definitive role in the explanation of consumer choice and its undeveloped philosophical basis limits its attempt to explain economic behaviour. The nature of neuroeconomics is explored, especially with respect to what it reveals about the valuation of alternatives, choice and emotion. The tendency of human consumers to discount future rewards illustrates how behavioural and neuroscientific accounts of choice contribute to psychological explanations of choice and the issues this raises for both routine everyday choices and more extreme compulsions. Central to this is the phenomenon of matching in which consumers tend to select the immediately larger or largest reward and the neurophysiological and behavioural bases of this choice. Recognition that rewards are evoked by reinforcement contingencies and that the rewards themselves engender emotional responses via classical conditioning enhances understanding the contribution of neurological activity to the explanation of consumer behaviour. It is argued that neuroeconomics can play a vital explanatory role by providing an evolutionarily consistent warrant for the ascription of intentionality. The Behavioural Perspective Model is used as a template for investigations of consumer choice that lead to iterative theoretical development, forming the basis of a neurophilosophy in which neuroeconomics can find a decisive role