scholarly journals Risdiplam distributes and increases SMN protein in both the central nervous system and peripheral organs

2018 ◽  
Vol 6 (6) ◽  
pp. e00447 ◽  
Author(s):  
Agnès Poirier ◽  
Marla Weetall ◽  
Katja Heinig ◽  
Franz Bucheli ◽  
Kerstin Schoenlein ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Peripheral Organs ◽  
The Central Nervous System ◽  
Smn Protein

scholarly journals Neuroinvasion in Prion Diseases: The Roles of Ascending Neural Infection and Blood Dissemination

2010 ◽  
Vol 2010 ◽  
pp. 1-16 ◽  
Author(s):  
Sílvia Sisó ◽  
Lorenzo González ◽  
Martin Jeffrey
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Prion Protein ◽  
Prion Diseases ◽  
Autonomic Nerves ◽  
Peripheral Organs ◽  
Prion Strains ◽  
New Variant ◽  
Jakob Disease ◽  
The Central Nervous System

Prion disorders are infectious, neurodegenerative diseases that affect humans and animals. Susceptibility to some prion diseases such as kuru or the new variant of Creutzfeldt-Jakob disease in humans and scrapie in sheep and goats is influenced by polymorphisms of the coding region of the prion protein gene, while other prion disorders such as fatal familial insomnia, familial Creutzfeldt-Jakob disease, or Gerstmann-Straussler-Scheinker disease in humans have an underlying inherited genetic basis. Several prion strains have been demonstrated experimentally in rodents and sheep. The progression and pathogenesis of disease is influenced by both genetic differences in the prion protein and prion strain. Some prion diseases only affect the central nervous system whereas others involve the peripheral organs prior to neuroinvasion. Many experiments undertaken in different species and using different prion strains have postulated common pathways of neuroinvasion. It is suggested that prions access the autonomic nerves innervating peripheral organs and tissues to finally reach the central nervous system. We review here published data supporting this view and additional data suggesting that neuroinvasion may concurrently or independently involve the blood vascular system.

EFFECT OF SEROTONIN AND NEUROPEPTIDES ON ADENYLATE CYCLASE OF THE CENTRAL NERVOUS SYSTEM AND PERIPHERAL ORGANS OF THE FRESHWATER SNAIL PLANORBARIUS CORNEUS

1996 ◽  
Vol 28 (4) ◽  
pp. 417-424 ◽  
Author(s):  
MARIA ENRICA FERRETTI ◽  
DARIO SONETTI ◽  
MARIA CRISTINA PARESCHI ◽  
MARCO BUZZI ◽  
MARIA LUISA COLAMUSSI ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Adenylate Cyclase ◽  
Freshwater Snail ◽  
Planorbarius Corneus ◽  
Peripheral Organs ◽  
The Central Nervous System

Biochemical properties and kinetic parameters of dihydroxyphenyialanine – 5-hydroxytryptophan decarboxylase in brain, liver, and adrenals of cat

1979 ◽  
Vol 57 (7) ◽  
pp. 1014-1018 ◽  
Author(s):  
Sylvie Bouchard ◽  
Andrée G. Roberge
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Enzyme Activity ◽  
Kinetic Parameters ◽  
Biochemical Properties ◽  
Mechanisms Of Action ◽  
Decarboxylase Activity ◽  
Peripheral Organs ◽  
Exogenous Addition ◽  
The Central Nervous System

Biochemical properties and kinetic parameters of nonpurified dihydroxyphenylaianine –5-hydroxytryptophan decarboxylase extracted from brain and two peripheral organs, liver and adrenals, were studied in the cat. This study shows that decarboxylase activity in brain is lower than in peripheral organs and that 5-hydroxytryptophan can be decarboxylated without exogenous addition of pyridoxal-5′-phosphate (PLP). However, the addition of PLP substantially increases the enzyme activity. Excess of coenzyme (>60 μM) induces inhibition in adrenals and liver but not in the central nervous system (CNS). The observed inhibition might be related to the presence of a tetrahydroisoquinoline derivative formed in the medium. Differentiation between mechanisms of action of decarboxylase in the CNS and peripheral organs is suggested.

scholarly journals The Roles of GABA in Ischemia-Reperfusion Injury in the Central Nervous System and Peripheral Organs

2019 ◽  
Vol 2019 ◽  
pp. 1-19 ◽  
Author(s):  
Chaoran Chen ◽  
Xiang Zhou ◽  
Jialiang He ◽  
Zhenxing Xie ◽  
Shufang Xia ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Vital Role ◽  
Pathological Process ◽  
Peripheral Organs ◽  
Multiple Organs ◽  
Long Time ◽  
The Central Nervous System

Ischemia-reperfusion (I/R) injury is a common pathological process, which may lead to dysfunctions and failures of multiple organs. A flawless medical way of endogenous therapeutic target can illuminate accurate clinical applications. γ-Aminobutyric acid (GABA) has been known as a marker in I/R injury of the central nervous system (mainly in the brain) for a long time, and it may play a vital role in the occurrence of I/R injury. It has been observed that throughout cerebral I/R, levels, syntheses, releases, metabolisms, receptors, and transmissions of GABA undergo complex pathological variations. Scientists have investigated the GABAergic enhancers for attenuating cerebral I/R injury; however, discussions on existing problems and mechanisms of available drugs were seldom carried out so far. Therefore, this review would summarize the process of pathological variations in the GABA system under cerebral I/R injury and will cover corresponding probable issues and mechanisms in using GABA-related drugs to illuminate the concern about clinical illness for accurately preventing cerebral I/R injury. In addition, the study will summarize the increasing GABA signals that can prevent I/R injuries occurring in peripheral organs, and the roles of GABA were also discussed correspondingly.

Distribution of α-bungarotoxin binding sites in the central nervous system and peripheral organs of the rat

Toxicon ◽  
1978 ◽  
Vol 16 (3) ◽  
pp. 245-251 ◽  
Author(s):  
Nisson Schechter ◽  
Indhira C. Handy ◽  
Leo Pezzementi ◽  
Jakob Schmidt
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Binding Sites ◽  
Peripheral Organs ◽  
The Central Nervous System

Role of membrane complement regulators in neuromyelitis optica

2015 ◽  
Vol 21 (13) ◽  
pp. 1644-1654 ◽  
Author(s):  
Samira Saadoun ◽  
Marios C Papadopoulos
Keyword(s):  
Central Nervous System ◽  
Endothelial Cells ◽  
Nervous System ◽  
Neuromyelitis Optica ◽  
Normal Brain ◽  
Peripheral Organs ◽  
Cell Processes ◽  
Cultured Human Cells ◽  
The Central Nervous System ◽  
Complement Regulators

Background: It is unclear why AQP4-IgG primarily causes central nervous system lesions by activating complement, but generally spares peripheral AQP4-expressing organs. Objectives: To determine whether peripheral AQP4-expressing cells are protected from complement-mediated damage by expressing complement regulators. Methods: Human tissue and cultured human cells were immunostained for aquaporin-4 (AQP4), CD46, CD55 and CD59. We also determined the vulnerability to AQP4-IgG and complement-mediated damage of astrocytes cultured alone or co-cultured with endothelial cells. Results: In normal brain, astrocyte end-feet express AQP4, but are devoid of CD46, CD55 and CD59. Immunoreactivity for CD46, CD55 and CD59 is not increased in or around neuromyelitis optica lesions. In kidney AQP4 is co-expressed with CD46 and CD55, in stomach AQP4 is co-expressed with CD46 and in skeletal muscle AQP4 is co-expressed with CD46. Astrocytes cultured alone co-express AQP4 and CD59 but, in astrocyte-endothelial co-cultures, AQP4 is found in cell processes devoid of CD59. Astrocytes co-cultured with endothelial cells are more vulnerable to AQP4-IgG and complement-mediated lysis than astrocytes cultured alone. Conclusions: Complement regulators protect peripheral organs, but not the central nervous system, from AQP4-IgG and complement-mediated damage. Our findings may explain why neuromyelitis optica primarily damages the central nervous system, but spares peripheral organs.

scholarly journals Genome and stress-reaction in animals and humans

2018 ◽  
Vol 16 (1) ◽  
pp. 4-26 ◽  
Author(s):  
Natalya A. Dyuzhikova ◽  
Eugene V. Daev
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Physiological State ◽  
Current Data ◽  
Point Of View ◽  
Target Cells ◽  
Structural Genomic ◽  
Genomic Changes ◽  
Peripheral Organs ◽  
The Central Nervous System

Current data on the effects of stress at the level of the cell genomes of the central nervous system and peripheral organs in animals are discussed. Regulatory and structural genomic changes in the cells of the central nervous system under stress are considered as a mechanism for regulating the functions of the brain and peripheral organs that form the organism manifestations of stress. Based on the Yu.Ya. Kerkis and M.E. Lobashev point of view, we consider stress as a special physiological state of the nervous system, affecting the work and integrity of the genome in target cells in animals, and thus playing a major role in microevolutionary transformations.

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