scholarly journals ON THE RELATION BETWEEN LOSS OF FUNCTION AND STRUCTURAL CHANGE IN FOCAL LESIONS OF THE CENTRAL NERVOUS SYSTEM, WITH SPECIAL REFERENCE TO SECONDARY DEGENERATION

Brain ◽  
1907 ◽  
Vol 29 (4) ◽  
pp. 514-523 ◽  
Author(s):  
GORDON HOLMES
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Structural Change ◽  
Special Reference ◽  
Loss Of Function ◽  
Focal Lesions ◽  
Secondary Degeneration ◽  
The Central Nervous System

scholarly journals Insights Into the Role of CSF1R in the Central Nervous System and Neurological Disorders

2021 ◽  
Vol 13 ◽  
Author(s):  
Banglian Hu ◽  
Shengshun Duan ◽  
Ziwei Wang ◽  
Xin Li ◽  
Yuhang Zhou ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurological Disorders ◽  
Neurological Diseases ◽  
Colony Stimulating Factor ◽  
Loss Of Function ◽  
Axonal Spheroids ◽  
The Central Nervous System ◽  
Stimulating Factor

The colony-stimulating factor 1 receptor (CSF1R) is a key tyrosine kinase transmembrane receptor modulating microglial homeostasis, neurogenesis, and neuronal survival in the central nervous system (CNS). CSF1R, which can be proteolytically cleaved into a soluble ectodomain and an intracellular protein fragment, supports the survival of myeloid cells upon activation by two ligands, colony stimulating factor 1 and interleukin 34. CSF1R loss-of-function mutations are the major cause of adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) and its dysfunction has also been implicated in other neurodegenerative disorders including Alzheimer’s disease (AD). Here, we review the physiological functions of CSF1R in the CNS and its pathological effects in neurological disorders including ALSP, AD, frontotemporal dementia and multiple sclerosis. Understanding the pathophysiology of CSF1R is critical for developing targeted therapies for related neurological diseases.

Design, fabrication, and testing of a bioprinted nerve graft

2016 ◽  
Author(s):  
◽  
Christopher M. Owens
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Nerve Graft ◽  
Loss Of Function ◽  
Vitro Assay ◽  
Central Nervous System Damage ◽  
In Vivo Animal Model ◽  
The Central Nervous System

Injuries to nerves vary in their consequences, from weakened sensation and motor function to partial or complete paralysis. In the latter case, affecting about twenty thousand Americans yearly, the injury is debilitating and results in a significant decrease in quality of life. Currently there is no effective treatment for damage to the central nervous system, in particular the spinal cord. Compared to the injuries to the central nervous system, damage in the peripheral nerves, is more common, with about sixty thousand occurrences annually. The cost of associated surgical procedures and due to loss of function is in the billions. In this thesis we present work towards the construction and testing of a fully cellular, patented nerve graft, one amongst the first of its kind. For the fabrication of the graft we are the first to employ bioprinting (either implemented through a special purpose 3D bioprinter or manually), a novel tissue engineering method rapidly gaining acceptance and utility. We first review the status of bioprinting. We then detail the fabrication process. Next we report on the testing of the graft in an in vivo animal model through electrophysiology and histology. This is followed by the introduction of a novel in vitro model, aimed at providing a fast, inexpensive and reliable method to test engineered nerve grafts. We describe our work on the optimization of the in vitro assay and then the testing of the graft using the optimized assay. We conclude with a summary of our accomplishments and make suggestions for some exciting future applications of our approach.

Actinomycotic granuloma of the Gasserian ganglion with primary site in a dental root

1981 ◽  
Vol 54 (4) ◽  
pp. 553-555 ◽  
Author(s):  
Enrico Perna ◽  
R. Liguori ◽  
G. Petrone ◽  
E. Mannarino
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Special Reference ◽  
Unusual Case ◽  
Primary Site ◽  
Pathological Diagnosis ◽  
Gasserian Ganglion ◽  
Content Type ◽  
The Central Nervous System ◽  
Fine Print

✓ An unusual case of cerebral actinomycosis of the Gasserian ganglion is reported. The location and the pathological diagnosis of granuloma are both extremely rare. The literature is briefly reviewed with special reference to similar reports. The manner of spread and the course of the disease are described. The present case tends to confirm the opinion that primary cerebral actinomycosis is extremely rare and probably does not exist. The case also definitely indicates that the organism reaches the central nervous system by way of nerve or perineural pathways.

scholarly journals A novel Dbl family RhoGEF promotes Rho-dependent axon attraction to the central nervous system midline in Drosophila and overcomes Robo repulsion

2001 ◽  
Vol 155 (7) ◽  
pp. 1117-1122 ◽  
Author(s):  
Greg J. Bashaw ◽  
Hailan Hu ◽  
Catherine D. Nobes ◽  
Corey S. Goodman
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Rho Gtpases ◽  
Ectopic Expression ◽  
Nucleotide Exchange ◽  
Loss Of Function ◽  
Guanine Nucleotide Exchange ◽  
Positive Regulators ◽  
The Central Nervous System ◽  
Rho Gef

The key role of the Rho family GTPases Rac, Rho, and CDC42 in regulating the actin cytoskeleton is well established (Hall, A. 1998. Science. 279:509–514). Increasing evidence suggests that the Rho GTPases and their upstream positive regulators, guanine nucleotide exchange factors (GEFs), also play important roles in the control of growth cone guidance in the developing nervous system (Luo, L. 2000. Nat. Rev. Neurosci. 1:173–180; Dickson, B.J. 2001. Curr. Opin. Neurobiol. 11:103–110). Here, we present the identification and molecular characterization of a novel Dbl family Rho GEF, GEF64C, that promotes axon attraction to the central nervous system midline in the embryonic Drosophila nervous system. In sensitized genetic backgrounds, loss of GEF64C function causes a phenotype where too few axons cross the midline. In contrast, ectopic expression of GEF64C throughout the nervous system results in a phenotype in which far too many axons cross the midline, a phenotype reminiscent of loss of function mutations in the Roundabout (Robo) repulsive guidance receptor. Genetic analysis indicates that GEF64C expression can in fact overcome Robo repulsion. Surprisingly, evidence from genetic, biochemical, and cell culture experiments suggests that the promotion of axon attraction by GEF64C is dependent on the activation of Rho, but not Rac or Cdc42.

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