thumbnail

Walter de Gruyter GmbH

  2081-3856

  2081-6936

 

Cơ quản chủ quản:  De Gruyter Open Ltd. , DE GRUYTER POLAND SP Z O O

Lĩnh vực:
Neuroscience (miscellaneous)

Các bài báo tiêu biểu

Social cognition in major depressive disorder: A new paradigm?
- 2013
Pablo Billeke, Samantha Boardman, P. Murali Doraiswamy
Abstract

Social cognition refers to the brain mechanisms by which we process social information about other humans and ourselves. Alterations in interpersonal and social functioning are common in major depressive disorder, though only poorly addressed by current pharmacotherapies. Further standardized tests, such as depression ratings or neuropsychologic tests, used in routine practice provide very little information on social skills, schemas, attributions, stereotypes and judgments related to social interactions. In this article, we review recent literature on how healthy human brains process social decisions and how these processes are altered in major depressive disorder. We especially focus on interactive paradigms (e.g., game theory based tasks) that can reproduce daily life situations in laboratory settings. The evidences we review, together with the rich literature on the protective role of social networks in handling stress, have implications for developing more ecologically-valid biomarkers and interventions in order to optimize functional recovery in depressive disorders.

Tumour necrosis factor - alpha mediated mechanisms of cognitive dysfunction
- 2012
Bernhard T. Baune, Marie-Lou Camara, Harris A. Eyre, Catharine Jawahar, Helen Anscomb, Heinrich Körner
Abstract
Mitochondrial bioenergetics is defective in presymptomatic Tg2576 AD Mice
- 2011
Merina Varghese, Wei Zhao, Jun Wang, Ann‐Joy Cheng, Xiang Qian, Amna Chaudhry, Lap Ho, Giulio Maria Pasinetti
Abstract

Alzheimer’s disease (AD) is an age-related dementia, with the pathological hallmarks of neuritic plaques and neurofibrillary tangles, brain atrophy and loss of synaptic terminals. Dysfunctional mitochondrial bioenergetics is implicated as a contributing factor to the cognitive decline observed in AD. We hypothesized that, in the presence of the AD neurotoxic peptide beta-amyloid, mitochondrial respiration is impaired early in synaptic terminals, which are vital to cognitive performance, preferentially in cognitive centers of the brain. We compared oxygen consumption in synaptosomal and perikaryal mitochondria prepared from the cerebral cortex and cerebellum of wild type (WT) and AD transgenic Tg2576 mice. Compared to WT mice, Tg2576 mice showed decreased mitochondrial respiration in the cerebral cortex specifically in synaptosomal fraction, while the perikaryal mitochondria were unaffected. Neither mitochondrial fraction was affected in the cerebellum of Tg2576 mice as compared to WT. The occurrence of a bioenergetic defect in synaptic terminals of mice overexpressing mutant beta-amyloid, in particular in an area of the brain important to cognition, points to an early role of mitochondrial defects in the onset of cognitive deficits in AD.

Cortical surface complexity in a population-based normative sample
- 2014
Brynn A. Dombroski, Matthew Nitzken, Ahmed Elnakib, Fahmi Khalifa, Andrew E. Switala, Ayman El-Baz, Manuel F. Casanova
Abstract

MRI studies on abnormal brain development are dependent on the quality, quantity, and type of normative development data available for comparison. Limitations affecting previous studies on normative development include small sample sizes, lack of demographic representation, heterogeneous subject populations, and inadequate longitudinal data. The National Institutes of Health Pediatric MRI Data Repository (NIHPD) for normative development was designed to address the aforementioned issues in reliability measures of control subjects for comparison studies. The subjects were recruited from six Pediatric Study Centers nationwide to create the largest, non-biased, longitudinal database of the developing brain. Using the NIHPD, we applied a 3D shape analysis method involving spherical harmonics to identify the cortical surface complexity of 396 subjects (210 female; 186 male) between the ages of 4.8 y and 22.3 y. MRI data had been obtained at one, two, or three time points approximately two years apart. A total of 144 participants (79 female; 65 male) provided MRI data from all time points. Our results confirm a direct correlation between cortical complexity and age in both males and females. Additionally, within the examined age range, females displayed consistently and significantly greater cortical complexity than males. Findings suggest that the underlying neural circuitry within male and female brains is different, possibly explaining observations of sexual dimorphism in social interaction, communication, and higher cognitive processes.

Towards dynamical network biomarkers in neuromodulation of episodic migraine
- 2013
Markus Dahlem, Sebastian Rode, Arne May, Naoya Fujiwara, Yoshito Hirata, Kazuyuki Aihara, Jürgen Kurths
Abstract

Computational methods have complemented experimental and clinical neurosciences and led to improvements in our understanding of the nervous systems in health and disease. In parallel, neuromodulation in form of electric and magnetic stimulation is gaining increasing acceptance in chronic and intractable diseases. In this paper, we firstly explore the relevant state of the art in fusion of both developments towards translational computational neuroscience. Then, we propose a strategy to employ the new theoretical concept of dynamical network biomarkers (DNB) in episodic manifestations of chronic disorders. In particular, as a first example, we introduce the use of computational models in migraine and illustrate on the basis of this example the potential of DNB as early-warning signals for neuromodulation in episodic migraine.

Oskar Vogt: The first myeloarchitectonic map of the human frontal cortex
- 2010
Miloš Judaš, Maja Cepanec
Abstract

The aim of this paper is threefold: (a) to provide the translation in English of Oskar Vogt’s seminal 1910 paper describing the first myeloarchitectonic map of the human frontal cortex, introduced by a brief historical review of Cécile & Oskar Vogt’s contribution to neuroscience; (b) to provide an annotated bibliography of major works of cortical cytoarchitectonics and myeloarchitectonics in the tradition of the Brodmann-Vogt architectonic school (Supplement 2); and (c) to provide an annotated bibliography of major works of the Russian architectonic school which was founded by Oskar Vogt (Supplement 3).

Breath-hold diving as a brain survival response
- 2013
Željko Dujić, Toni Brešković, Darija Baković
Abstract

Elite breath-hold divers are unique athletes challenged with compression induced by hydrostatic pressure and extreme hypoxia/hypercapnia during maximal field dives. The current world records for men are 214 meters for depth (Herbert Nitsch, No-Limits Apnea discipline), 11:35 minutes for duration (Stephane Mifsud, Static Apnea discipline), and 281 meters for distance (Goran Čolak, Dynamic Apnea with Fins discipline). The major physiological adaptations that allow breath-hold divers to achieve such depths and duration are called the “diving response” that is comprised of peripheral vasoconstriction and increased blood pressure, bradycardia, decreased cardiac output, increased cerebral and myocardial blood flow, splenic contraction, and preserved O2 delivery to the brain and heart. This complex of physiological adaptations is not unique to humans, but can be found in all diving mammals. Despite these profound physiological adaptations, divers may frequently show hypoxic loss of consciousness. The breath-hold starts with an easy-going phase in which respiratory muscles are inactive, whereas during the second so-called “struggle” phase, involuntary breathing movements start. These contractions increase cerebral blood flow by facilitating left stroke volume, cardiac output, and arterial pressure. The analysis of the compensatory mechanisms involved in maximal breath-holds can improve brain survival during conditions involving profound brain hypoperfusion and deoxygenation.

Arousal from slices to humans
- 2010
Nebojsa Kezunovic, Christen Simon, James Hyde, Kristen Smith, Paige Beck, Angela K. Odle, Edgar García‐Rill
Abstract

Most psychiatric and neurological disorders exhibit sleep disorders, and in some cases presage the disease. Study of the control of sleep and waking has the potential for making a major impact on a number of disorders, making translational neuroscience research on this area critical. One element of the reticular activating system (RAS) is the pedunculopontine nucleus (PPN), which is the cholinergic arm of the RAS, and projects to the thalamus to trigger thalamocortical rhythms and to the brainstem to modulate muscle tone and locomotion. We developed a research program using brainstem slices containing the PPN to tell us about the cellular and molecular organization of this region. In addition, we developed the P13 midlatency auditory evoked potential, which is generated by PPN outputs, preparation in freely moving rats. This allows the study of PPN cellular and molecular mechanisms at the level of the whole animal. We also study the P50 midlatency auditory evoked potential, which is the human equivalent of the rodent P13 potential, allowing us to study processes detected in vitro, confirmed in the whole animal, and tested in humans. This translational research program led to the discovery of a novel mechanism of sleep-wake control, pointing the way to a number of new clinical applications in the development of novel stimulants and anesthetics.

Cyclic AMP-specific PDEs: A promising therapeutic target for CNS repair
- 2010
Mousumi Ghosh, Damien D. Pearse
Abstract

Research to date has indicated that cAMPspecific PDEs, particularly the members of PDE4 family, play a crucial role in the pathogenesis of CNS injury and neurodegeneration by downregulating intracellular levels of cAMP in various cell types. Reduced cAMP signaling results in immune cell activation, inflammation, secondary tissue damage, scar formation and axon growth failure, ultimately leading to an exacerbation of injury, the prevention of endogenous repair and limited functional recovery. Although inhibition of cAMPspecific-PDE activity through the use of drugs like Rolipram has been shown to reverse these deficiencies and mediate neurorepair, an inability to develop selective agents and/or reduce dose-limiting side-effects associated with PDE4 inhibition has hampered their clinical translation. Recent work with more selective pharmacological inhibitors of cAMP-specific PDEs and molecular targeting approaches, along with improved understanding of the basic biology and role of PDEs in pathological processes may enable this promising therapeutic approach to advance clinically and have a similar impact on CNS injury and disease as PDE5 inhibitors have had on the treatment of sexual dysfunction.

Gerstmann-Straüssler-Scheinker PRNP P102L-129V mutation
Tập 2 Số 1 - 2011
Isidro Ferrer, Margarita Carmona, Rosa Blanco, María Jesús Rey Recio, R. M. San Segundo
Abstract

Neuropathological and biochemical studies in a case of Gerstmann-Straüssler-Scheinker disease bearing the PRNP P102L-129V mutation showed numerous multicentric PrPres in the cerebral cortex, striatum, thalamus and cerebellum, PrPres globular deposits in the anterior and posterior horns of the spinal cord, and multiple granular PrPres deposits in the grey and white matter of the encephalon and spinal cord. Western blots with antiPrPres antibodies revealed several weak bands ranging from 36 to 66 kDa, weak bands of 29 and 24 kDa, a strong band of about 20 kDa, a low band of molecular weight around 15 kDa and a weaker band of about 7 kDa. Spongiform degeneration was absent. Hyper-phosphorylated 3R and 4R tau occurred in dystrophic neurites surrounding PrPres plaques, neuropil threads and, to a lesser degree, in the form of neurofibrillary tangles. Gel electrophoresis of sarkosyl-insoluble fractions and western blotting with anti-phospho-tau antibodies showed a pattern similar to that seen in Alzheimer disease cases run in parallel. Dystrophic neurites in the vicinity of PrPres plaques were enriched in voltage dependent anion channel thus suggesting abnormal accumulation of mitochondria. These changes were associated with increased oxidative damage in neurons and astrocytes, Finally, increased expression of active stress kinases, that have the capacity to phosphorylate tau in vitro, p38 (p-38-P) and SAPK/ JNK (SAPK/JNK-P) was found in cell processes surrounding PrP plaques. Together, these observations provide evidences of mitochondrial abnormalities, and increased oxidative stress damage and oxidative stress responses in GSS bearing the PRNP P102L-129V mutation.