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Nervous system
About: Nervous system is a research topic. Over the lifetime, 16729 publications have been published within this topic receiving 847181 citations.
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614 citations
Patent•
22 Aug 2002
TL;DR: In this article, a family of neuronal migration-inducing, proliferation-promoting and neurite outgrowth promoting factors, termed NRP compounds, were described and described for the treatment of brain injury and neurodegenerative disease.
Abstract: The invention discloses a family of neuronal migration-inducing, proliferation-promoting and neurite outgrowth promoting factors, termed NRP compounds, and provides compositions and methods for the use of NRP compounds in the treatment of brain injury and neurodegenerative disease. NRP-1 compounds induce neurons and neuroblasts to proliferate and migrate into areas of damage caused by acute brain injury or chronic neurodegenerative disease, such as stroke, trauma, nervous system infections, demyelinating diseases, dementias, and metabolic disorders. NRP compounds may be administered directly to a subject or to a subject's cells by a variety of means including orally, intraperitoneally, intravascularly, and directly into the nervous system of a patient.
613 citations
TL;DR: GAP-43 is established as an intrinsic presynaptic determinant for neurite outgrowth and plasticity by targeting constitutive expression of the growth-associated protein GAP- 43 to the neurons of adult transgenic mice.
612 citations
TL;DR: There is much evidence that autonomic control of the airways may be abnormal in airway disease, particularly in asthma, but the precise role of neural mechanisms in the pathogenesis of air-flow obstruction and bronchial hyperresponsiveness remains to be defined.
Abstract: Several aspects of airway function are under autonomic control: airway smooth muscle tone, submucosal gland secretion, epithelial cell function, bronchial vascular tone and permeability, and probably secretion from mast cells and other inflammatory cells. Neural control of human airways is more complex than previously recognized. In addition to afferent nerves and cholinergic adrenergic mechanisms (including circulating catecholamines), there are nonadrenergic, noncholinergic nerves that may be both excitatory and inhibitory. The neurotransmitters of this third nervous system are uncertain, but there is some evidence that neuropeptides may be involved. Several neuropeptides have recently been identified in human airways and, although they have potent effects, their pathophysiologic role is uncertain. There is much evidence that autonomic control of the airways may be abnormal in airway disease, particularly in asthma, but the precise role of neural mechanisms in the pathogenesis of air-flow obstruction and bronchial hyperresponsiveness remains to be defined.
611 citations
TL;DR: It is shown that in two mouse models of motoneuron disease, axons of fast-fatiguable motoneurons are affected synchronously, long before symptoms appear, and that mot oneuron disease involves predictable, selective vulnerability patterns by physiological subtypes of axons, episodes of abrupt pruning in the target region and compensation by resistant axons.
Abstract: Neurodegenerative diseases can have long preclinical phases and insidious progression patterns, but the mechanisms of disease progression are poorly understood. Because quantitative accounts of neuronal circuitry affected by disease have been lacking, it has remained unclear whether disease progression reflects processes of stochastic loss or temporally defined selective vulnerabilities of distinct synapses or axons. Here we derive a quantitative topographic map of muscle innervation in the hindlimb. We show that in two mouse models of motoneuron disease (G93A SOD1 and G85R SOD1), axons of fast-fatiguable motoneurons are affected synchronously, long before symptoms appear. Fast-fatigue-resistant motoneuron axons are affected at symptom-onset, whereas axons of slow motoneurons are resistant. Axonal vulnerability leads to synaptic vesicle stalling and accumulation of BC12a1-a, an anti-apoptotic protein. It is alleviated by ciliary neurotrophic factor and triggers proteasome-dependent pruning of peripheral axon branches. Thus, motoneuron disease involves predictable, selective vulnerability patterns by physiological subtypes of axons, episodes of abrupt pruning in the target region and compensation by resistant axons.
611 citations