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Schizotypy is a latent organisation of a cluster of personality styles, such as magical thinking, disorganisation and anhedonia, which are in the normal range of the psychosis continuum. Schizotypy relates to an increased likelihood of perceiving expressed emotion (EE). EE is characterised by criticism, rejection, and emotional over-involvement and less warmth from a close relative. Neuroimaging studies have found normal frontal lobe activation to EE-criticism in people with high schizotypy. Alternatively, electroencephalography measures emotion processing, such as frontal theta power and occipital alpha power. Frontal theta power responds to cognitive and affective processes and occipital alpha power denotes less consciousness and emotional attention. This study aimed to determine the relation of these electroencephalography responses during criticism and praise to perceived emotional support. Participants (n = 32) representing the full (low-to-high) range of positive schizotypy listened to and rated the self-relevance of EE-like criticism and praise and affectively neutral comments while undergoing electroencephalography. Participants completed self-report measures of schizotypy, depression and anxiety. A subset of those with a high positive schizotypy score (n = 22) completed a measure of perceived EE - lack of emotional support. Higher perceived EE - lack of emotional support correlated with lower frontal theta power and lower occipital alpha power during criticism and praise in schizotypal participants. The findings suggest that these neural responses may relate to less perceived emotional support in people with high schizotypy, of which a reduction of frontal theta power denotes less emotional arousal and lower occipital alpha power denotes more alertness to emotional information may relate to less perceived emotional support in people with high schizotypy., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Rationale: The gut-brain axis includes bidirectional communication between intestinal microbiota and the central nervous system. Bifidobacterium and Lactobacillus spp. have been implicated in psychological health, such as depression, through various pathways (e.g. inflammation). Research needs a better understanding of direct and indirect effects through examination of psychological factors that make people susceptible to, or offer protection against, depression., Objective: This study investigated the relationships between gut microbiota, inflammation and psychological risk and resilience factors for depression., Methods: Forty participants (13 m/27 f) recruited from the general population completed self-report questionnaires for depression, self-judgement, over-identification and affective and cognitive empathy. Faecal and blood samples were taken to assay microbiota (Bifidobacterium; Lactobacillus spp.) and pro-inflammatory molecules (C-reactive protein, CRP and interleukin-6, IL-6), respectively., Results: Hierarchical regression analyses (controlling for sex, age and the shared variance of risk and resilience factors) showed that (i) cognitive depression was significantly predicted by negative self-judgement and reduced cognitive empathy; (ii) abundance of Lactobacillus spp. was directly related to positive self-judgement but only indirectly to cognitive depression and lower affective empathy (both through self-judgement); and (iii) CRP was the strongest predictor of reduced cognitive empathy, with suppression effects seen for age (negative) and IL-6 (positive) after controlling for CRP., Conclusions: Findings suggest that lactobacilli and inflammation may be differentially associated with mood disorder via brain mechanisms underpinning self-judgement and cognitive empathy, respectively. Further trials investigating interventions to increase Lactobacillus spp. in depression would benefit from direct measures of self-judgement and affective empathic distress, whilst those that aim to reduce inflammation should investigate cognitive empathy.

Modified RNA molecules have recently been shown to regulate nervous system functions. This mini-review and associated mini-symposium provide an overview of the types and known functions of novel modified RNAs in the nervous system, including covalently modified RNAs, edited RNAs, and circular RNAs. We discuss basic molecular mechanisms involving RNA modifications as well as the impact of modified RNAs and their regulation on neuronal processes and disorders, including neural fate specification, intellectual disability, neurodegeneration, dopamine neuron function, and substance use disorders., (Copyright © 2014 the authors 0270-6474/14/3415170-08$15.00/0.)

Adrenomedullin is a multifunctional amidated peptide that has been found in most nuclei of the CNS, where it plays a neuromodulatory role. An adrenomedullin binding protein has recently been found in plasma and characterized as complement factor H. This regulator of the complement system inhibits the progression of the complement cascade and modulates the function of adrenomedullin. Our study shows the ample distribution of factor H immunoreactivity in neurons of telencephalon, diencephalon, mesencephalon, pons, medulla, and cerebellum in the rat CNS, using immunohistochemical techniques for both light and electron microscopy. Factor H immunoreactivity was found in the cytoplasm, but nuclear staining was also a common finding. Some blood vessels and glial cells were also immunoreactive for factor H. Colocalization studies by double immunofluorescence followed by confocal microscopy revealed frequent coexistence of factor H and adrenomedullin immunoreactivities, thus providing morphological evidence for the potential interaction of these molecules in the CNS. The presence of factor H immunoreactivity in glial cells was confirmed by colocalization with glial fibrillary acidic protein. In summary, factor H is highly expressed in the CNS where it could play important roles in regulating adrenomedullin actions and contributing to an intracerebral complement system.

This work examines the age-related changes of the NO pathway in the central nervous system (CNS), analyzing nitric oxide synthase (NOS) isoform expression, the level of nitrotyrosine-modified proteins, and the NOS activity in the cerebral cortex, decorticated brain (basal ganglia, thalamus, hypothalamus, tegtum and tegmentum) and cerebellum of young, adult and aged rats. Our data demonstrate that the different NOS isoforms are not uniformly expressed across the CNS. In this sense, the nNOS and eNOS isoenzymes are expressed mainly in the cerebellum and decorticated brain, respectively, while the iNOS isoenzyme shows the highest level in cerebellum. Concerning age, in the cerebral cortex nNOS significantly increased its expression only in adult animals; meanwhile, in the cerebellum the eNOS expression decreased whereas iNOS increased in adult and aged rats. No age-related changes in any isoform were found in decorticated brain. NOS activity, determined by nitrate plus nitrite quantification, registered the highest levels in the cerebellum, where the significant increase detected with aging was probably related to iNOS activity. The number of nitrotyrosine-modified immunoreactive bands differed among regions; thus, the highest number was detected in the decorticated brain while the cerebellum showed the least number of bands. Finally, bulk protein nitration increased in cerebral cortex only in adult animal. No changes were found in the decorticated brain, and the decrease detected in the cerebellum of aged animals was not significant. According to these results, the NO pathway is differently modified with age in the three CNS regions analyzed., (Copyright 2002 Elsevier Science B.V.)

Adrenomedullin (AM) is a novel vasodilator peptide first purified from human pheochromocytoma by tracing its capacity to stimulate cAMP production in platelets. AM immunoreactivity is widely distributed in the central nervous system (CNS) and in the rat has been demonstrated by immunohistochemical techniques to be present in many neurons throughout the brain and spinal cord, as well as in some vascular endothelial cells and perivascular glial cells. Electron microscopy shows that the immunoreactivity is located mainly in the neuronal cytoplasm, but also occurs in the cell nucleus in some cells of the caudate putamen and olfactory tubercle. Biochemical analyses suggest that higher molecular forms, presumably precursor forms, may predominate over fully processed AM in some brain areas. The expression of AM immunoreactivity is increased in cortical neurons, endothelial cells, and perivascular processes after a simulation of ischemia by oxygen and glucose deprivation. Immunohistochemical, electrophysiological, and pharmacological studies suggest that AM in the CNS can act as a neurotransmitter, neuromodulator, or neurohormone, or as a cytoprotective factor in ischemic/hypoxic conditions, in addition to its vasodilator role., (Copyright 2002 Wiley-Liss, Inc.)

Nitric oxide (NO) has been recognized as a key regulatory factor in many physiological processes, including central nervous system function, development, and phatophysiology. NO is produced by a class of enzymes known as NO synthases (NOS) and in normal adult animals only the neuronal isoform (nNOS) is detectable. During cortical development, nNOS was found at E14 in neuroblasts of the marginal zone and its expression raised to a zenith by P5, decreasing afterwards until reaching a steady level by P10. At that time, nNOS was found mainly in pyramidal neurons. Interestingly, the inducible isoform of the enzyme (iNOS) was also active from P3 to P7, but it disappeared almost completely by P20. The neurodegeneration observed during normal aging and following hypoxic accidents seems to be the result of cumulative free radical damage, and excessive production of NO may be at the basis of the cascade. After ischemic events we observed an elevation in the number of neurons expressing nNOS coincident with an elevation in Ca2+-dependent NOS activity for up to 120 min. After this period, nNOS activity began to decrease but it was substituted by a rapid increase in Ca2+-independent activity coincident with the histological appearance of previously undetectable iNOS-immunoreactive neurons. These increases in NO production were accompanied by specific patterns of protein nitration, a process that seems to result in loss of protein function. In particular, we observed a correlation between exposure to ischemia-reperfusion and nitration of cytochrome c. This process was coincident with the exit of the cytochrome from the mitochondria to the surrounding cytoplasm, an early event in neuronal apoptosis. Interestingly, most of the morphological and molecular changes associated with ischemic damage were prevented by treatment with inhibitors of NO production, indicating a clear path in the search for efficacious drugs in the battle against cerebrovascular accidents.

Since traditional electrical brain signal analysis is mostly qualitative, the development of new quantitative methods is crucial for restricting the subjectivity in the study of brain signals. These methods are particularly fruitful when they are strongly correlated with intuitive physical concepts that allow a better understanding of brain dynamics. Here, new method based on orthogonal discrete wavelet transform (ODWT) is applied. It takes as a basic element the ODWT of the EEG signal, and defines the relative wavelet energy, the wavelet entropy (WE) and the relative wavelet entropy (RWE). The relative wavelet energy provides information about the relative energy associated with different frequency bands present in the EEG and their corresponding degree of importance. The WE carries information about the degree of order/disorder associated with a multi-frequency signal response, and the RWE measures the degree of similarity between different segments of the signal. In addition, the time evolution of the WE is calculated to give information about the dynamics in the EEG records. Within this framework, the major objective of the present work was to characterize in a quantitative way functional dynamics of order/disorder microstates in short duration EEG signals. For that aim, spontaneous EEG signals under different physiological conditions were analyzed. Further, specific quantifiers were derived to characterize how stimulus affects electrical events in terms of frequency synchronization (tuning) in the event related potentials.

Objective: A review about the possible cellular and molecular mechanisms of aging and related neurodegenerative diseases., Development: The mechanisms involved in neuronal decrease, connectivity losses and glial reactivity, detected both in neurodegenerative (Alzheimer's disease) and physiological aging, are analyzed from the morphological and histological point of view to provide the morphofunctional base of the cognitive and intellectual alterations characterizing the senescence process. Taken together, these data are correlated to the possible genetical aspects implied in this process, reviewing the most relevant results on senescence and cellular death obtained from yeast, fruit fly and nematodes; besides this, a brief review of the molecular biology of gerontogenes was carried out, and the possible mechanisms inducing aging and neurodegenerative processes are analyzed according to the state-of-the-art related theories. Finally, cellular, biochemical and genetical data are correlated in the signal transduction way implied in the increase of the intracellular calcium level as the starting point of cell death., Conclusions: The main process implied in the neuronal cell death responsible for aging and the related neurodegenerative diseases are started by different agents such as the lacking of neurotrophic factors, hypoxia, hypoglycemia, excitotoxicity, and oxygen and nitrogen free radicals.

Sandhoff's disease is a severe form of gangliosidosis GM2 which presents in the first year of life, basically as progressive psychomotor retardation and/or a macular red cherry spot. Our patient presented the clinical picture characteristic of the disease. Diagnosis was confirmed by determining the activity of hexosaminidases A and B in serum and of beta-N-acetil hexosaminases in fibroblast culture. In view of the fatal prognosis of the disease, in 1991 a transplant of alogenic bone marrow (TMO) was carried out to try to replace the enzymes. This required exhaustive radiological follow-up to determine the possible neuro-radiological changes seen in this storage disease. Although treatment was not successful, the neuro-radiological findings may be of interest as perhaps being characteristic of the GM2 gangliosidosis: 1. Bilateral thalamic hyperecogenity in the cerebral ecography. 2. Differences between the thalamo-putamen densities due to bilateral homogeneous thalamic hyperdensity on the CT scan. 3. Thalamic hypointensity both on T2 sequences and in proton density on MR with the cerebral white matter being progressively affected. In conclusion, we suggest that bilateral symmetrical thalamic changes are an early finding which is probably specific to the GM2 gangliosidoses and may be useful from the point of view of carrying out more specific investigations in infants suspected of having a degenerative neurological disorder.