The international Jihadism: A new type of threat and regional cooperation as a remedy

The capture of Mosul and the ensuing blitzkrieg of the Islamic State of Iraq and the Levant (ISIL) over the Sunni majority region of Syria and Iraq reminded the world of the seriousness of the threat posed by the Salafist-jihadists. By connecting the tactic of “the management of savagery” with external resources and links, ISIL seems to have succeeded in materializing the full potential that the new type of conflict can pose to the existing international order. The “New War”, as formulated by Mary Kaldor, is the product of the dual erosion of nation states that globalization has brought about. Due to the growing malfunctioning of nation states, it becomes more difficult to secure the governmental monopoly of organized violence and border control, while there is also the internationalization of criminal groups’ networks. So far, the U.S.-led coalition has waged war against ISIL, but the strategy based on older thinking about national security helps to proliferate ISIL-type threats rather than to contain them. One of the main reasons of the failure lies in the context that the U.S. administration has been supporting extremist networks as tools to subvert the regime it does not want. This is attested to by the fact that the ISIL is the end product of U.S. covert interventions in Afghanistan, Bosnia, Chechnya, Iraq and Syria. Therefore, a different type of remedy is necessary. The article assesses the effectiveness of concerted policing and the exchange of intelligence of the Shanghai Cooperation Organization in its fight against the Islamic terrorism in Central Asia and concludes that a regional cooperation based on pragmatic and limited purposes, rather than a military alliance based on some shared values, is a better model to cope with the new type of threats as represented by ISIL. Such regional cooperation has the potential to bring about more stable administration and provides the ground of economic stability as it gives its member states more resilience to the outside political pressures that are detrimental to the fight against terrorism, in addition to giving them the grounds for economic development with the purpose of mutual benefits.Publisher's Versio

GSK-3β Is Required for Memory Reconsolidation in Adult Brain

Activation of GSK-3β is presumed to be involved in various neurodegenerative diseases, including Alzheimer's disease (AD), which is characterized by memory disturbances during early stages of the disease. The normal function of GSK-3β in adult brain is not well understood. Here, we analyzed the ability of heterozygote GSK-3β knockout (GSK+/−) mice to form memories. In the Morris water maze (MWM), learning and memory performance of GSK+/− mice was no different from that of wild-type (WT) mice for the first 3 days of training. With continued learning on subsequent days, however, retrograde amnesia was induced in GSK+/− mice, suggesting that GSK+/− mice might be impaired in their ability to form long-term memories. In contextual fear conditioning (CFC), context memory was normally consolidated in GSK+/− mice, but once the original memory was reactivated, they showed reduced freezing, suggesting that GSK+/− mice had impaired memory reconsolidation. Biochemical analysis showed that GSK-3β was activated after memory reactivation in WT mice. Intraperitoneal injection of a GSK-3 inhibitor before memory reactivation impaired memory reconsolidation in WT mice. These results suggest that memory reconsolidation requires activation of GSK-3β in the adult brain

P301S Mutant Human Tau Transgenic Mice Manifest Early Symptoms of Human Tauopathies with Dementia and Altered Sensorimotor Gating

Tauopathies are neurodegenerative disorders characterized by the accumulation of abnormal tau protein leading to cognitive and/or motor dysfunction. To understand the relationship between tau pathology and behavioral impairments, we comprehensively assessed behavioral abnormalities in a mouse tauopathy model expressing the human P301S mutant tau protein in the early stage of disease to detect its initial neurological manifestations. Behavioral abnormalities, shown by open field test, elevated plus-maze test, hot plate test, Y-maze test, Barnes maze test, Morris water maze test, and/or contextual fear conditioning test, recapitulated the neurological deficits of human tauopathies with dementia. Furthermore, we discovered that prepulse inhibition (PPI), a marker of sensorimotor gating, was enhanced in these animals concomitantly with initial neuropathological changes in associated brain regions. This finding provides evidence that our tauopathy mouse model displays neurofunctional abnormalities in prodromal stages of disease, since enhancement of PPI is characteristic of amnestic mild cognitive impairment, a transitional stage between normal aging and dementia such as Alzheimer's disease (AD), in contrast with attenuated PPI in AD patients. Therefore, assessment of sensorimotor gating could be used to detect the earliest manifestations of tauopathies exemplified by prodromal AD, in which abnormal tau protein may play critical roles in the onset of neuronal dysfunctions

The making of ''Black Hand'' reconsidered

This study assesses the effects of Serbian „Macedonian Struggle“ over the making of the secret society, popularly known as „Black Hand.“ Building on the existent literature, by using memoires, court records and sources from diplomatic correspondence, the articles traces a decade of metamorphosis of secret society of officers from the 1903 May coup until the end of Balkan wars 1913, emphasizing the previously neglected Macedonian aspect, deemed here crucial for understanding the functioning of the society and its relation to the Serbian state

Imaging Multimodalities for Dissecting Alzheimer\u27s Disease: Advanced Technologies of Positron Emission Tomography and Fluorescence Imaging.

The rapid progress in advanced imaging technologies has expanded our toolbox for monitoring a variety of biological aspects in living subjects including human. In vivo radiological imaging using small chemical tracers, such as with positron emission tomography, represents an especially vital breakthrough in the efforts to improve our understanding of the complicated cascade of neurodegenerative disorders including Alzheimer\u27s disease (AD), and it has provided the most reliable visible biomarkers for enabling clinical diagnosis. At the same time, in combination with genetically modified animal model systems, the most recent innovation of fluorescence imaging is helping establish diverse applications in basic neuroscience research, from single-molecule analysis to animal behavior manipulation, suggesting the potential utility of fluorescence technology for dissecting the detailed molecular-based consequence of AD pathophysiology. In this review, our primary focus is on a current update of PET radiotracers and fluorescence indicators beneficial for understanding the AD cascade, and discussion of the utility and pitfalls of those imaging modalities for future translational research applications. We will also highlight current cutting-edge genetic approaches and discuss how to integrate individual technologies for further potential innovations

Tau Fibril Formation in Cultured Cells Compatible with a Mouse Model of Tauopathy

Neurofibrillary tangles composed of hyperphosphorylated tau protein are primarily neuropathological features of a number of neurodegenerative diseases collectively termed tauopathy. To understand the mechanisms underlying the cause of tauopathy, precise cellular and animal models are required. Recent data suggest that the transient introduction of exogenous tau can accelerate the development of tauopathy in the brains of non-transgenic and transgenic mice expressing wild-type human tau. However, the transmission mechanism leading to tauopathy is not fully understood. In this study, we developed cultured-cell models of tauopathy representing a human tauopathy. Neuro2a (N2a) cells containing propagative tau filaments were generated by introducing purified tau fibrils. These cell lines expressed full-length (2N4R) human tau and the green fluorescent protein (GFP)-fused repeat domain of tau with P301L mutation. Immunocytochemistry and super-resolution microscopic imaging revealed that tau inclusions exhibited filamentous morphology and were composed of both full-length and repeat domain fragment tau. Live-cell imaging analysis revealed that filamentous tau inclusions are transmitted to daughter cells, resulting in yeast-prion-like propagation. By a standard method of tau preparation, both full-length tau and repeat domain fragments were recovered in sarkosyl insoluble fraction. Hyperphosphorylation of full-length tau was confirmed by the immunoreactivity of phospho-Tau antibodies and mobility shifts by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). These properties were similar to the biochemical features of P301L mutated human tau in a mouse model of tauopathy. In addition, filamentous tau aggregates in cells barely co-localized with ubiquitins, suggesting that most tau aggregates were excluded from protein degradation systems, and thus propagated to daughter cells. The present cellular model of tauopathy will provide an advantage for dissecting the mechanisms of tau aggregation and degradation and be a powerful tool for drug screening to prevent tauopathy