Novel Modality of GSK-3 Inhibition For Treating Neurodegeneration
DOI: 10.29245/2572.942X/2018/6.1227 View / Download PdfIdo Rippin, Hagit Eldar-Finkelman*
Department of Human Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv University, Israel
Vagal-Immune Interactions in the Control of Hypertension
Renata M. Lataro1, Helio C. Salgado2*
1Department of Physiological Sciences, Center of Biological Sciences, Federal University of Santa Catarina, Florianópolis, Santa Catarina, Brazil
2Department of Physiology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo, Brazil
There is a consensus in the literature that the autonomic dysfunction in arterial hypertension involves the increase of sympathetic activity and, also, reduction of vagal tone. In the last years, the role played by inflammation in the development of hypertension and target organs injuries, such as heart and blood vessels, has been emphasized. Although the clinical importance of sympathetic hyperactivity and its treatment of arterial hypertension is recognized, the therapeutic benefit of increasing parasympathetic activity in hypertensive patients still requires an in-depth investigation. The increased vagal activity may produce beneficial effects on cardiovascular modulation and inflammation, preventing target organ damage. Parasympathetic neurotransmission can be improved by the inhibition of acetylcholinesterase action. Anticholinesterase agents prevent the hydrolysis of acetylcholine by acetylcholinesterase, prolonging its availability within the cholinergic cleft. This article will highlight the key concepts of the cardiac autonomic imbalance and the increase of acetylcholine availability under inflammation and control of arterial hypertension. In conclusion, significant evidence exists associating the reduction of parasympathetic activity and the occurrence of inflammation involving the pathophysiology of hypertension; suggesting that the improvement of vagal activity by the increased availability of acetylcholine has a remarkable potential for the therapeutic intervention on arterial hypertension.
DOI: 10.29245/2572.942X/2018/6.1226 View / Download Pdf Persistent Antigens Hypothesis: The Human Leukocyte Antigen (HLA) Connection
DOI: 10.29245/2572.942X/2018/6.1235 View / Download PdfLisa M. James1,2,3, Apostolos P. Georgopoulos1,2,3,4*
1Brain Sciences Center, Department of Veterans Affairs Health Care System, Minneapolis, MN, 55417, USA
2Department of Neuroscience, University of Minnesota Medical School, Minneapolis, MN 55455, USA
3Department of Psychiatry, University of Minnesota Medical School, Minneapolis, MN 55455, USA
4Department of Neurology, University of Minnesota Medical School, Minneapolis, MN 55455, USA
Commentary: Pleiotropic Neuropathological and Biochemical Alterations associated with Myo5a Mutation in a Rat Model
DOI: 10.29245/2572.942X/2018/6.1231 View / Download PdfGeorge Stoica1*, Heidi Martini-Stoica2
1Texas A&M University, College Station, TX,USA
2Baylor College of Medicine, Houston, TX, USA
Recent Advances in the Biology of BDNF And the Newly Identified Pro-Peptide
Toshiyuki Mizui1, 2*, Masami Kojima1,2,3#
Biomedical Research Inst. (BMD), National Institute of Advanced Industrial Science and Technology (AIST), 1-8-31 Midorioka, Ikeda, Osaka, 563-8577 Japan
Core Research for Evolutional Science and Technology (CREST), Science and Technology Agency (JST), Kawaguchi, 332-0012, Japan
Graduate School of Frontier Bioscience, Osaka University, Suita 565-0871, Japan
Most growth factors are initially synthesized as precursors. To produce biologically active mature peptides, the pro-domain is cleaved by proteolytic processing. However, compared with mature bioactive growth factors, the biological roles of pro-domains are poorly understood. Recent new findings on brain-derived neurotrophic factor (BDNF), a growth factor in the brain that promotes neuronal survival, differentiation, and synaptic plasticity, have been reported. Interestingly, the pro-domain (pro-peptide) of BDNF is endogenously present and localized at presynaptic termini, where it surprisingly functions as a facilitator of long-term depression (LTD). Given that BDNF elicits synaptic transmission and long-term potentiation (LTP), BDNF and its pro-peptide might exert distinct roles in synaptic plasticity in the central nervous system (CNS). In addition to reports on the BDNF pro-peptide, we review recent literature on the role of BDNF in the peripheral nervous system (PNS), and in brain-body interactions following exercise. Together, these findings provide new insight into BDNF biology.
DOI: 10.29245/2572.942X/2018/6.1228 View / Download Pdf Neurotransmitters and their Receptors as the Upstream Regulators of the Most Common Human Cancers and their Stem Cells
DOI: 10.29245/2572.942X/2018/6.1230 View / Download PdfHildegard M. Schuller
Department of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville TN, USA