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Progress in Neurobiology

Masoud Ghodrati, Seyed-Mahdi Khaligh-Razavi, Sidney R Lehky
The lateral geniculate nucleus (LGN) has often been treated in the past as a linear filter that adds little to retinal processing of visual inputs. Here we review anatomical, neurophysiological, brain imaging, and modeling studies that have in recent years built up a much more complex view of LGN. These include effects related to nonlinear dendritic processing, cortical feedback, synchrony and oscillations across LGN populations, as well as involvement of LGN in higher level cognitive processing Although recent studies have provided valuable insights into early visual processing including the role of LGN, a unified model of LGN responses to real-world objects has not yet been developed...
June 17, 2017: Progress in Neurobiology
Hassan Bukhari, Annika Glotzbach, Katharina Kolbe, Gregor Leonhardt, Christina Loosse, Thorsten Müller
Alzheimer's disease (AD) is the most common neurodegenerative disease with tens of millions of people affected worldwide. The pathogenesis is still poorly understood and various therapeutical approaches targeting the amyloid β (Aβ) peptide, a product of the amyloidogenic cleavage of the amyloid precursor protein (APP), failed. Moreover, a couple of studies critically questioned the relevance of Aβ in the pathogenesis of AD. Thus, new ideas need to be studied and one highly interesting hypothesis is the APP mediated signal transduction to the nucleus...
June 3, 2017: Progress in Neurobiology
Achim Peters, Bruce S McEwen, Karl Friston
The term 'stress' - coined in 1936 - has many definitions, but until now has lacked a theoretical foundation. Here we present an information-theoretic approach - based on the 'free energy principle' - defining the essence of stress; namely, uncertainty. We address three questions: What is uncertainty? What does it do to us? What are our resources to master it? Mathematically speaking, uncertainty is entropy or 'expected surprise'. The 'free energy principle' rests upon the fact that self-organizing biological agents resist a tendency to disorder and must therefore minimize the entropy of their sensory states...
May 30, 2017: Progress in Neurobiology
Jonathan A Coles, Elmarie Myburgh, James M Brewer, Paul G McMenamin
Rapid progress is being made in understanding the roles of the cerebral meninges in the maintenance of normal brain function, in immune surveillance, and as a site of disease. Most basic research on the meninges and the neural brain is now done on mice, major attractions being the availability of reporter mice with fluorescent cells, and of a huge range of antibodies useful for immunocytochemistry and the characterization of isolated cells. In addition, two-photon microscopy through the unperforated calvaria allows intravital imaging of the undisturbed meninges with sub-micron resolution...
May 25, 2017: Progress in Neurobiology
S Monteiro, S Roque, F Marques, M Correia-Neves, J J Cerqueira
Interferon gamma (IFNγ) is a pro-inflammatory cytokine, first described as a secreted molecule capable of interfering with viral replication. Since then, numerous other important actions in the context of the immune response to invading pathogens (including those invading the brain) have been ascribed to this pleiotropic cytokine. Nevertheless, the precise role of IFNγ in neuropsychiatric and neurodegenerative disorders, and its possible contribution to the regulation of normal brain function, remains enigmatic...
May 18, 2017: Progress in Neurobiology
Ben Loos, Daniel J Klionsky, Esther Wong
Accumulation of toxic protein aggregates in the nerve cells is a hallmark of neuronal diseases and brain aging. Mechanisms to enhance neuronal surveillance to improve neuronal proteostasis have a direct impact on promoting neuronal health and forestalling age-related decline in brain function. Autophagy is a lysosomal degradative pathway pivotal for neuronal protein quality control. Different types of autophagic mechanisms participate in protein handling in neurons. Macroautophagy targets misfolded and aggregated proteins in autophagic vesicles to the lysosomes for destruction, while chaperone-mediated autophagy (CMA) degrades specific soluble cytosolic proteins delivered to the lysosomes by chaperones...
May 11, 2017: Progress in Neurobiology
Ana O Pires, F G Teixeira, B Mendes-Pinheiro, Sofia C Serra, Nuno Sousa, António J Salgado
Parkinson's disease (PD) is a neurodegenerative disorder characterized by the degeneration of dopaminergic neurons and/or loss od neuronal projections, in several dopaminergic networks. Current treatments for idiopathic PD rely mainly on the use of pharmacologic agents to improve motor symptomatology of PD patients. Nevertheless, so far PD remains an incurable disease. Therefore, it is of utmost importance to establish new therapeutic strategies for PD treatment. Over the last 20 years, several molecular, gene and cell/stem-cell therapeutic approaches have been developed with the aim of counteracting or retarding PD progression...
April 27, 2017: Progress in Neurobiology
Haiying Li, Jiang Wu, Haitao Shen, Xiyang Yao, Chenglin Liu, S Pianta, J Han, C V Borlongan, Gang Chen
Accumulating evidence advances the critical role of autophagy in brain pathology after stroke. Investigations employing autophagy induction or inhibition using pharmacological tools or autophagy-related gene knockout mice have recently revealed the biological significance of intact and functional autophagy in stroke. Most of the reported cases attest to a pro-survival role for autophagy in stroke, by facilitating removal of damaged proteins and organelles, which can be recycled for energy generation and cellular defenses...
April 13, 2017: Progress in Neurobiology
Anusha Mohan, Sven Vanneste
It is suggested that the brain undergoes plastic changes in order to adapt to changing environmental needs. Sensory deprivation results in decreased input to the brain leading to adaptive or maladaptive changes. Although several theories hypothesize the mechanism of these adaptive and maladaptive changes, the course of action taken by the brain heavily depends on the age of incidence of damage. The growing body of literature on the topic proposes that maladaptive changes in the brain are instrumental in creating phantom percepts, defined as the perception of a sensory experience in the absence of a physical stimulus...
April 11, 2017: Progress in Neurobiology
Dumisile Lumkwana, Andre du Toit, Craig Kinnear, Ben Loos
Neurodegenerative diseases are characterised by the presence of cytoplasmic and nuclear protein aggregates that result in toxicity and neuronal cell death. Autophagy is a physiological cellular process that engulfs primarily long-lived proteins as well as protein aggregates with subsequent cargo delivery for lysosomal degradation. The rate at which the material is degraded through autophagy is referred to as autophagic flux. Although we have progressed substantially in unravelling the role and regulation of the autophagy machinery, its dysfunction in pathology as well as its dynamic changes in the disease progression remains largely unclear...
April 3, 2017: Progress in Neurobiology
Shiraz Tyebji, Anthony J Hannan
Dementia encapsulates a set of symptoms that include loss of mental abilities such as memory, problem solving or language, and reduces a person's ability to perform daily activities. Alzheimer's disease is the most common form of dementia, however dementia can also occur in other neurological disorders such as Huntington's disease (HD). Many studies have demonstrated that loss of neuronal cell function manifests pre-symptomatically and thus is a relevant therapeutic target to alleviate symptoms. Synaptopathy, the physiological dysfunction of synapses, is now being approached as the target for many neurological and psychiatric disorders, including HD...
April 2, 2017: Progress in Neurobiology
Sandrine Passemard, Franck Perez, Emilie Colin-Lemesre, Sowmyalakshmi Rasika, Pierre Gressens, Vincent El Ghouzzi
The Golgi apparatus plays a central role in cell homeostasis, not only in processing and maturing newly synthesized proteins and lipids but also in orchestrating their sorting, packing, routing and recycling on the way to their final destination. These multiple secretory pathways require a complex ballet of vesicular and tubular carriers that continuously bud off from donor membranes and fuse to acceptor membranes. Membrane trafficking is particularly prominent in axons, where cargo molecules have a long way to travel before they reach the synapse, and in oligodendrocytes, which require an immense increase in membrane surface in order to sheathe axons in myelin...
April 2, 2017: Progress in Neurobiology
Maria Trinidad Herrero, Micaela Morelli
No abstract text is available yet for this article.
August 2017: Progress in Neurobiology
Stefano Gustincich, Silvia Zucchelli, Antonello Mallamaci
The post-genomic era has unveiled the existence of a large repertory of non-coding RNAs and repetitive elements that play a fundamental role in cellular homeostasis and dysfunction. These may represent unprecedented opportunities to modify gene expression at the right time in the correct space in vivo, providing an almost unlimited reservoir of new potential pharmacological agents. Hijacking their mode of actions, the druggable genome can be extended to regulatory RNAs and DNA elements in a scalable fashion...
August 2017: Progress in Neurobiology
Maria Egle De Stefano, Maria Trinidad Herrero
Matrix metalloproteinases (MMPs) are a large family of ubiquitous extracellular endopeptidases, which play important roles in a variety of physiological and pathological conditions, from the embryonic stages throughout adult life. Their extraordinary physiological "success" is due to concomitant broad substrate specificities and strict regulation of their expression, activation and inhibition levels. In recent years, MMPs have gained increasing attention as significant effectors in various aspects of central nervous system (CNS) physiology...
August 2017: Progress in Neurobiology
Marta C Antonelli, María Eugenia Pallarés, Sandra Ceccatelli, Stefan Spulber
There is a large consensus that the prenatal environment determines the susceptibility to pathological conditions later in life. The hypothesis most widely accepted is that exposure to insults inducing adverse conditions in-utero may have negative effects on the development of target organs, disrupting homeostasis and increasing the risk of diseases at adulthood. Several models have been proposed to investigate the fetal origins of adult diseases, but although these approaches hold true for almost all diseases, particular attention has been focused on disorders related to the central nervous system, since the brain is particularly sensitive to alterations of the microenvironment during early development...
August 2017: Progress in Neurobiology
Valerie Joers, Malú G Tansey, Giovanna Mulas, Anna R Carta
Over the last decade the important concept has emerged that microglia, similar to other tissue macrophages, assume different phenotypes and serve several effector functions, generating the theory that activated microglia can be organized by their pro-inflammatory or anti-inflammatory and repairing functions. Importantly, microglia exist in a heterogenous population and their phenotypes are not permanently polarized into two categories; they exist along a continuum where they acquire different profiles based on their local environment...
August 2017: Progress in Neurobiology
Chai K Lim, Francisco J Fernández-Gomez, Nady Braidy, Cristina Estrada, Cristina Costa, Silvia Costa, Alban Bessede, Emiliano Fernandez-Villalba, Anna Zinger, Maria Trinidad Herrero, Gilles J Guillemin
Parkinson's disease (PD) is a common neurodegenerative disorder characterized by loss of dopaminergic neurons and localized neuroinflammation occurring in the midbrain several years before the actual onset of symptoms. Neuroinflammation leads to microglia activation and release of a large number of proinflammatory mediators. The kynurenine pathway (KP) of tryptophan catabolism is one of the major regulators of the immune response and is also likely to be implicated in the inflammatory and neurotoxic events in Parkinsonism...
August 2017: Progress in Neurobiology
Dora Reglodi, Justine Renaud, Andrea Tamas, Yousef Tizabi, Sergio B Socías, Elaine Del-Bel, Rita Raisman-Vozari
Parkinson's disease is a progressive neurodegenerative disorder characterized by the degeneration of midbrain nigral dopaminergic neurons. Although its etiology remains unknown, the pathological role of several factors has been highlighted, namely oxidative stress, neuroinflammation, protein misfolding, and mitochondrial dysfunction, in addition to genetic predispositions. The current therapy is mainly symptomatic with l-DOPA aiming to replace dopamine. Novel therapeutic approaches are being investigated with the intention of influencing pathways leading to neuronal death and dysfunction...
August 2017: Progress in Neurobiology
Amber L Marriott, Edgardo Rojas-Mancilla, Paola Morales, Mario Herrera-Marschitz, R Andrew Tasker
It is now well established that many of society's most devastating and costly neurological diseases and disorders arise from trauma at, or shortly after birth. In some cases deficits are seen in childhood and in others they are substantially delayed; arising in adolescence or young adulthood. In either case the initial insult initiates a metabolic and/or neurodegenerative cascade that proceeds, often undetected, for a considerable period of time before diagnosable symptoms appear. This affords a potential for detecting and slowing or arresting degenerative and/or malfunctioning processes prior to the appearance of symptoms, but requires an understanding of the mechanisms involved in the progressive dysfunction that characterizes the disease progression process...
August 2017: Progress in Neurobiology
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