Lipofuscin pigment in neurons of young mice with a hereditary central nervous system defect

1970 ◽  
Vol 128 (3) ◽  
pp. 359-365 ◽  
Author(s):  
W. Keith O'steen ◽  
Kalidas Nandy
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
System Defect ◽  
Lipofuscin Pigment ◽  
Young Mice

The Pathology of Gomen Disease: A Cerebellar Disorder of Horses in New Caledonia

1982 ◽  
Vol 19 (4) ◽  
pp. 399-405 ◽  
Author(s):  
W. J. Hartley ◽  
T. Kuberski ◽  
G. LeGonidec ◽  
P. Daynes
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Purkinje Cells ◽  
New Caledonia ◽  
Cerebellar Disorder ◽  
Lipofuscin Pigment ◽  
The Central Nervous System

The lesions of Gomen disease consist of widespread loss of Purkinje cells with extensive deposition of lipofuscin pigment in neurones in most areas of the central nervous system. We suggest these two disease processes are related and the entity may be an acquired environmental neuronal lipofuscinosis.

RISK OF CENTRAL-NERVOUS SYSTEM DEFECT

The Lancet ◽  
1967 ◽  
Vol 289 (7488) ◽  
pp. 507-508
Author(s):  
J. Lorber ◽  
C.O. Carter ◽  
J.A.Fraser Roberts
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
System Defect

scholarly journals INFLUENCE OF HOST FACTORS ON NEUROINVASIVENESS OF VESICULAR STOMATITIS VIRUS

1937 ◽  
Vol 66 (1) ◽  
pp. 35-57 ◽  
Author(s):  
Albert B. Sabin ◽  
Peter K. Olitsky
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Sciatic Nerve ◽  
Vesicular Stomatitis Virus ◽  
Occipital Cortex ◽  
The Central Nervous System ◽  
Vesicular Stomatitis ◽  
Old Mice ◽  
Young Mice

1. Injection of vesicular stomatitis virus into the leg muscles of young mice gives rise to flaccid paralysis of the inoculated extremity as the first clinical sign of a disease which is invariably fatal; old mice similarly injected with the largest doses of virus survive without exhibiting any signs of illness. 2. In young mice the virus was shown to multiply at the site of inoculation and to invade the sciatic nerve and spinal cord; there was no evidence of multiplication of virus in the blood or viscera. 3. In old mice, after intramuscular injection of as much as 10 million M.C.L.D., there was no evidence of either local or systemic multiplication; in spite of the persistence of thousands of M.C.L.D. of virus at the site of inoculation for at least 4 days, there was no detectable invasion of the sciatic nerve or the central nervous system. 4. Injection of the virus directly into the sciatic nerve of old mice led to the typical paralytic disease in half the number of animals. 5. For 3 days after intrasciatic injection the virus could be demonstrated in the nerve but not in the spinal cord or brain. At the onset of paralysis (6th day) virus was detectable in the spinal cord but no longer in the inoculated nerve. 6. The capacity of the virus to invade the central nervous system from the nerve but not from the muscle suggested the existence of a barrier in the muscle or myoneural junction. 7. Injection of the virus into the vitreous humor of the eye is followed by a fatal encephalitis in 15 day old mice, but 1 year old mice, with few exceptions, survive without showing signs of disease. 8. The spread of virus in the brains of intraocularly injected, 15 day old mice was too rapid to indicate the pathways which were pursued, but in 21 day old mice there was evidence that the primary pathway was probably along the axons of the optic nerve with decussation to the contralateral diencephalon and mesencephalon, and subsequent early spread to the corresponding occipital cortex. In resistant, old mice, however, no virus was found in any part of the brain.

46,XY/46,XX blood chimerism with severe central nervous system defect and multiple congenital malformations

1986 ◽  
Vol 23 (3) ◽  
pp. 833-836
Author(s):  
Caroline Lieber ◽  
Joseph Bordiuk ◽  
Franklin Desposito ◽  
John M. Opitz ◽  
James F. Reynolds
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Congenital Malformations ◽  
System Defect

CONGENITAL DEFECTS OF THE CENTRAL NERVOUS SYSTEM ASSOCIATED WITH HYPERENDEMIC GOITER IN A NEOLITHIC HIGHLAND SOCIETY OF NETHERLANDS NEW GUINEA

PEDIATRICS ◽  
1962 ◽  
Vol 29 (3) ◽  
pp. 345-363
Author(s):  
D. Carleton Gajdusek
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
World Literature ◽  
New Guinea ◽  
Congenital Defects ◽  
Medical Problems ◽  
Central Nervous System Damage ◽  
System Defect ◽  
The Central Nervous System ◽  
Genetic And Environmental Factors

A recently discovered, isolated, and still neolithic population in the interior Highlands of Netherlands New Guinea has been studied, in which most, and perhaps all, of the members suffer from varying degrees of congenital central nervous system damage. This damage ranges from subtle degrees of mental subnormality to severe feeble-mindedness often associated with deafness or deaf-mutism. In this region about one-fourth of the males and two-thirds of the females are found to have goiter. In some hamlets the incidence reaches 100% among the adult females. Many of these goiters are among the largest reported in world literature. The extreme isolation and the high incidence of this congenital goitrous cretinism of varying degrees of severity make this region ideally suited for studies of both the genetic and environmental factors which determine the defects in this population. Similarly, they offer an unprecedented opportunity to investigate the etiology and pathogenesis of central nervous system defect associated with endemic goiter. The possibility that an unusual use of sweet potato leaves as a dietary staple in a region wherein the total nutritional balance is marginally adequate may play a role in the medical situation is under investigation. Metabolic and biochemical studies will be reported in subsequent papers in this series. Other medical problems of the area are briefly discussed and the distribution of goitrous areas in New Guinea is reviewed.

scholarly journals INFLUENCE OF HOST FACTORS ON NEUROINVASIVENESS OF VESICULAR STOMATITIS VIRUS

1938 ◽  
Vol 67 (2) ◽  
pp. 229-249 ◽  
Author(s):  
Albert B. Sabin ◽  
Peter K. Olitsky
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Vesicular Stomatitis Virus ◽  
Guinea Pigs ◽  
Central Nervous System Disease ◽  
Intracerebral Injection ◽  
Spinal Nerves ◽  
The Central Nervous System ◽  
Vesicular Stomatitis ◽  
Young Mice

Peripheral inoculation of vesicular stomatitis virus is constantly followed by myelitis or encephalitis in young mice, but not in young (or old) guinea pigs. The cause of this variation was elucidated by investigating the fate of the virus after inoculation by a number of different routes. Direct intracerebral injection of minimally infective amounts of virus was found to be equally fatal for young mice and young guinea pigs, indicating that the central nervous system as a whole was as easily injured by the virus in one species as in the other. The events following nasal instillation of the virus varied in young and old guinea pigs. While there appeared to be a transitory multiplication of virus in the nasal mucosa of both young and old, the central nervous system was regularly invaded only in the young. In these, virus was first found only in the anterior rhinencephalon; later it spread to the piriform and hippocampal (olfactory regions) but not to the neopallial portions of the cortex, and the only other area to exhibit virus was the diencephalon (including the pars optica hypothalami), where its further progression was apparently arrested. Absence of central nervous system disease following inoculation into sites supplied by spinal nerves (e.g. sciatic) was found to be due to inability of the virus to invade the nerves. Since direct intrasciatic inoculation frequently led to a fatal ascending myelitis, it was evident that the central nervous system could be invaded along the spinal nerves, and that they did not constitute the main barrier. Furthermore, since multiplication of virus was demonstrated in tissues supplied by the spinal nerves, a process of elimination made it seem possible that the specialized, terminal nerve endings might be the structures which prevent the progression of the virus from the infected tissues to the axons and hence also to the central nervous system. 7 day old guinea pigs (or guinea pigs as a species) were thus found to possess much the same type of barriers to the progression of peripherally inoculated vesicular stomatitis virus as are acquired by mice at a considerably later age. In a discussion of the present data, they have been correlated with known variations in neuroinvasiveness of other viruses and their bearing on the nature of inapparent or subclinical infections of the central nervous system has been considered.

Neurotropic enteroviruses co-opt “fair-weather-friend” commensal gut microbiota to drive host infection and central nervous system disturbances

2019 ◽  
Vol 42 ◽  
Author(s):  
Kevin B. Clark
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Gut Bacteria ◽  
Infection Cycle ◽  
Fair Weather ◽  
Host Health ◽  
Microbe Interactions ◽  
Animal Hosts ◽  
Host Infection ◽  
Neuropsychiatric Conditions

Abstract Some neurotropic enteroviruses hijack Trojan horse/raft commensal gut bacteria to render devastating biomimicking cryptic attacks on human/animal hosts. Such virus-microbe interactions manipulate hosts’ gut-brain axes with accompanying infection-cycle-optimizing central nervous system (CNS) disturbances, including severe neurodevelopmental, neuromotor, and neuropsychiatric conditions. Co-opted bacteria thus indirectly influence host health, development, behavior, and mind as possible “fair-weather-friend” symbionts, switching from commensal to context-dependent pathogen-like strategies benefiting gut-bacteria fitness.

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