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Progress in Neurobiology

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https://www.readbyqxmd.com/read/28528956/brain-interference-revisiting-the-role-of-ifn%C3%AE-in-the-central-nervous-system
#1
REVIEW
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
https://www.readbyqxmd.com/read/28502807/augmenting-brain-metabolism-to-increase-macro-and-chaperone-mediated-autophagy-for-decreasing-neuronal-proteotoxicity-and-aging
#2
REVIEW
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
https://www.readbyqxmd.com/read/28457671/old-and-new-challenges-in-parkinson-s-disease-therapeutics
#3
REVIEW
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
https://www.readbyqxmd.com/read/28456633/optineurin-in-amyotrophic-lateral-sclerosis-multifunctional-adaptor-protein-at-the-crossroads-of-different-neuroprotective-mechanisms
#4
REVIEW
Andrea Markovinovic, Raffaello Cimbro, Tereza Ljutic, Jasna Kriz, Boris Rogelj, Ivana Munitic
When optineurin mutations showed up on the amyotrophic lateral sclerosis (ALS) landscape in 2010, they differed from most other ALS-causing genes. They seemed to act by loss- rather than gain-of-function, and it was unclear how a polyubiquitin-binding adaptor protein, which was proposed to regulate a variety of cellular functions including cell signaling and vesicle trafficking, could mediate neuroprotection. This review discusses the considerable progress that has been made since then. A large number of mutations in optineurin and optineurin-interacting proteins TANK-binding kinase (TBK1) and p62/SQSTM-1 have been found in the ALS patients, suggesting a common neuroprotective pathway...
April 26, 2017: Progress in Neurobiology
https://www.readbyqxmd.com/read/28445713/deregulation-of-%C3%AE-synuclein-in-parkinson-s-disease-insight-from-epigenetic-structure-and-transcriptional-regulation-of-snca
#5
REVIEW
Subhrangshu Guhathakurta, Eugene Bok, Baggio A Evangelista, Yoon-Seong Kim
Understanding regulation of α-synuclein has long been a central focus for Parkinson's disease (PD) researchers. Accumulation of this protein in the Lewy body or neurites, mutations in the coding region of the gene and strong association of α-synuclein encoding gene multiplication (duplication/triplication) with familial form of PD have indicated the importance of this molecule in pathogenesis of the disease. Several years of research identified many potential faulty pathways associated with accumulation of α-synuclein inside dopaminergic neurons and its transmission to neighboring ones...
April 23, 2017: Progress in Neurobiology
https://www.readbyqxmd.com/read/28442394/granin-derived-peptides
#6
REVIEW
Josef Troger, Markus Theurl, Rudolf Kirchmair, Teresa Pasqua, Bruno Tota, Tommaso Angelone, Maria C Cerra, Yvonne Nowosielski, Raphaela Mätzler, Jasmin Troger, Jaur R Gayen, Vance Trudeau, Angelo Corti, Karen B Helle
The granin family comprises altogether 7 different proteins originating from the diffuse neuroendocrine system and elements of the central and peripheral nervous systems. The family is dominated by three uniquely acidic members, namely chromogranin A (CgA), chromogranin B (CgB) and secretogranin II (SgII). Since the late 1980s it has become evident that these proteins are proteolytically processed, intragranularly and/or extracellularly into a range of biologically active peptides; a number of them with regulatory properties of physiological and/or pathophysiological significance...
April 22, 2017: Progress in Neurobiology
https://www.readbyqxmd.com/read/28414101/autophagy-in-hemorrhagic-stroke-mechanisms-and-clinical-implications
#7
REVIEW
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
https://www.readbyqxmd.com/read/28408150/adaptive-and-maladaptive-neural-compensatory-consequences-of-sensory-deprivation-from-a-phantom-percept-perspective
#8
REVIEW
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
https://www.readbyqxmd.com/read/28392287/blocked-delayed-or-obstructed-what-causes-poor-white-matter-development-in-intrauterine-growth-restricted-infants
#9
REVIEW
Mary Tolcos, Steven Petratos, Jonathan J Hirst, Flora Wong, Sarah J Spencer, Aminath Azhan, Ben Emery, David W Walker
Poor white matter development in intrauterine growth restricted (IUGR) babies remains a major, untreated problem in neonatology. New therapies, guided by an understanding of the mechanisms that underlie normal and abnormal oligodendrocyte development and myelin formation, are required. Much of our knowledge of the mechanisms that underlie impaired myelination come from studies in adult demyelinating disease, preterm brain injury, or experimental models of hypoxia-ischemia. However relatively less is known for IUGR which is surprising because IUGR is a leading cause of perinatal mortality and morbidity, second only to premature birth...
April 6, 2017: Progress in Neurobiology
https://www.readbyqxmd.com/read/28385648/autophagic-flux-control-in-neurodegeneration-progress-and-precision-targeting-where-do-we-stand
#10
REVIEW
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
https://www.readbyqxmd.com/read/28377290/synaptopathic-mechanisms-of-neurodegeneration-and-dementia-insights-from-huntington-s-disease
#11
REVIEW
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
https://www.readbyqxmd.com/read/28377289/golgi-trafficking-defects-in-postnatal-microcephaly-the-evidence-for-golgipathies
#12
REVIEW
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
https://www.readbyqxmd.com/read/28342942/the-nature-of-early-astroglial-protection-fast-activation-and-signaling
#13
REVIEW
Julianna Kardos, László Héja, Katalin Jemnitz, Richárd Kovács, Miklós Palkovits
Our present review is focusing on the uniqueness of balanced astroglial signaling. The balance of excitatory and inhibitory signaling within the CNS is mainly determined by sharp synaptic transients of excitatory glutamate (Glu) and inhibitory γ-aminobutyrate (GABA) acting on the sub-second timescale. Astroglia is involved in excitatory chemical transmission by taking up i) Glu through neurotransmitter-sodium transporters, ii) K(+) released due to presynaptic action potential generation, and iii) water keeping osmotic pressure...
March 22, 2017: Progress in Neurobiology
https://www.readbyqxmd.com/read/28322920/stem-cell-transplantation-therapy-for-multifaceted-therapeutic-benefits-after-stroke
#14
REVIEW
Ling Wei, Zheng Z Wei, Michael Qize Jiang, Osama Mohamad, Shan Ping Yu
One of the exciting advances in modern medicine and life science is cell-based neurovascular regeneration of damaged brain tissues and repair of neuronal structures. The progress in stem cell biology and creation of adult induced pluripotent stem (iPS) cells has significantly improved basic and pre-clinical research in disease mechanisms and generated enthusiasm for potential applications in the treatment of central nervous system (CNS) diseases including stroke. Endogenous neural stem cells and cultured stem cells are capable of self-renewal and give rise to virtually all types of cells essential for the makeup of neuronal structures...
March 18, 2017: Progress in Neurobiology
https://www.readbyqxmd.com/read/28322921/linking-deregulation-of-non-coding-rna-to-the-core-pathophysiology-of-alzheimer-s-disease-an-integrative-review
#15
REVIEW
Mark J Millan
The human genome encodes a vast repertoire of protein non-coding RNAs (ncRNA), some specific to the brain. MicroRNAs, which interfere with the translation of target mRNAs, are of particular interest since their deregulation has been implicated in neurodegenerative disorders like Alzheimer's disease (AD). However, it remains challenging to link the complex body of observations on miRNAs and AD into a coherent framework. Using extensive graphical support, this article discusses how a diverse panoply of miRNAs convergently and divergently impact (and are impacted by) core pathophysiological processes underlying AD: neuroinflammation and oxidative stress; aberrant generation of β-amyloid-42 (Aβ42); anomalies in the production, cleavage and post-translational marking of Tau; impaired clearance of Aβ42 and Tau; perturbation of axonal organisation; disruption of synaptic plasticity; endoplasmic reticulum stress and the unfolded protein response; mitochondrial dysfunction; aberrant induction of cell cycle re-entry; and apoptotic loss of neurons...
March 17, 2017: Progress in Neurobiology
https://www.readbyqxmd.com/read/28274676/islet-amyloid-polypeptide-another-key-molecule-in-alzheimer-s-pathogenesis
#16
REVIEW
Yun Zhang, Weihong Song
Recent epidemiological evidence reveals that patients suffering from type 2 diabetes mellitus (T2DM) often experience a significant decline in cognitive function, and approximately 70% of those cases eventually develop Alzheimer's disease (AD). Although several pathological processes are shared by AD and T2DM, the exact molecular mechanisms connecting these two diseases are poorly understood. Aggregation of human islet amyloid polypeptide (hIAPP), the pathological hallmark of T2DM, has also been detected in brain tissue and is associated with cognitive decline and AD development...
March 6, 2017: Progress in Neurobiology
https://www.readbyqxmd.com/read/28268181/ethical-challenges-in-developing-drugs-for-psychiatric-disorders
#17
REVIEW
Felix Carrier, David Banayan, Randy Boley, Niranjan Karnik
As the classification of mental disorders advances towards a disease model as promoted by the National Institute of Mental Health (NIMH) Research Domain Criteria (RDoC), there is hope that a more thorough neurobiological understanding of mental illness may allow clinicians and researchers to determine treatment efficacy with less diagnostic variability. This paradigm shift has presented a variety of ethical issues to be considered in the development of psychiatric drugs. These challenges are not limited to informed consent practices, industry funding, and placebo use...
March 6, 2017: Progress in Neurobiology
https://www.readbyqxmd.com/read/28442128/challenges-in-developing-drugs-for-neurological-and-psychiatric-disorders
#18
EDITORIAL
Neal G Simon, Michael J Brownstein
No abstract text is available yet for this article.
May 2017: Progress in Neurobiology
https://www.readbyqxmd.com/read/27519538/new-drug-developments-in-psychosis-challenges-opportunities-and-strategies
#19
REVIEW
Matcheri S Keshavan, Ashley N Lawler, Henry A Nasrallah, Rajiv Tandon
All currently approved drugs for schizophrenia work mainly by dopaminergic antagonism. While they are efficacious for psychotic symptoms, their efficacy is limited for negative symptoms and cognitive deficits which underlie the substantive disability in this illness. Recent insights into the biological basis of schizophrenia, especially in relation to non-dopaminergic mechanisms, have raised the efforts to find novel and effective drug targets, though with relatively little success thus far. Potential impediments to novel drug discovery include the continued use of symptom based disease definitions which leads to etiological and pathophysiological heterogeneity, lack of valid preclinical models for drug testing, and design limitations in clinical trials...
May 2017: Progress in Neurobiology
https://www.readbyqxmd.com/read/27317387/familial-dysautonomia-history-genotype-phenotype-and-translational-research
#20
REVIEW
Lucy Norcliffe-Kaufmann, Susan A Slaugenhaupt, Horacio Kaufmann
Familial dysautonomia (FD) is a rare neurological disorder caused by a splice mutation in the IKBKAP gene. The mutation arose in the 1500s within the small Jewish founder population in Eastern Europe and became prevalent during the period of rapid population expansion within the Pale of Settlement. The carrier rate is 1:32 in Jews descending from this region. The mutation results in a tissue-specific deficiency in IKAP, a protein involved in the development and survival of neurons. Patients homozygous for the mutations are born with multiple lesions affecting mostly sensory (afferent) fibers, which leads to widespread organ dysfunction and increased mortality...
May 2017: Progress in Neurobiology
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