Immunological one-step determination of the central nervous system indicator proteins, neuron-specific enolase and glial fibrillary acidic protein, in meat products

2010 ◽  
Vol 54 (11) ◽  
pp. 1690-1695 ◽  
Author(s):  
Thorsten Kuczius ◽  
Olga Böhler ◽  
Helge Karch
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Glial Fibrillary Acidic Protein ◽  
Meat Products ◽  
Neuron Specific Enolase ◽  
Acidic Protein ◽  
The Central Nervous System ◽  
One Step

Identification of Central Nervous System Tissue in Retail Meat Products†

2000 ◽  
Vol 63 (2) ◽  
pp. 258-263 ◽  
Author(s):  
ERNST H. LÜCKER ◽  
ERICH EIGENBRODT ◽  
SABINE WENISCH ◽  
RUDI LEISER ◽  
MICHAEL BÜ]LTE
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Glial Fibrillary Acidic Protein ◽  
Meat Products ◽  
Neuron Specific Enolase ◽  
Cholesterol Content ◽  
Acidic Protein ◽  
Central Nervous System Tissue ◽  
Heat Treated ◽  
Retail Meat

A procedure to detect tissues from the central nervous system that involved quantification of cholesterol and immuno-chemical detection of neuron-specific enolase and glial fibrillary acidic protein was used to analyze 402 samples of heat-treated meat products from various food outlets in Germany. The cholesterol content of 16 samples (4.0%) indicated the possible presence of central nervous system tissue because the levels exceeded the normal maximum cholesterol content of cooked sausages. In 7 of these 16 heat-treated meat products, immunoblotting of both neuron-specific enolase and glial fibrillary acidic protein confirmed the presence of CNS tissue. Repeated sampling by veterinary officials and analysis by both cholesterol quantification and immunoblotting confirmed these findings. Whereas all of the control samples (with and without added central nervous system tissue) were correctly classified by both cholesterol quantification and immunoblotting, negative results of immunoblotting must be carefully interpreted in the case of intensively heat-treated meat products. Thus, studies have yet to establish an increase in sensitivity of immunoblotting of neuron-specific enolase and glial fibrillary acidic protein. However, the detection of illegal use of central nervous system tissue in heat-treated retail meat products demonstrates the need for suitable analytical methods to control transmissible encephalopathies and to enforce labeling laws.

scholarly journals Refining the concept of GFAP toxicity in Alexander disease

2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Albee Messing
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Glial Fibrillary Acidic Protein ◽  
Intermediate Filament ◽  
Alexander Disease ◽  
Acidic Protein ◽  
Sequence Variants ◽  
Main Body ◽  
Gain Of Function ◽  
The Central Nervous System

Abstract Background Alexander disease is caused by dominantly acting mutations in glial fibrillary acidic protein (GFAP), the major intermediate filament of astrocytes in the central nervous system. Main body In addition to the sequence variants that represent the origin of disease, GFAP accumulation also takes place, together leading to a gain-of-function that has sometimes been referred to as “GFAP toxicity.” Whether the nature of GFAP toxicity in patients, who have mixtures of both mutant and normal protein, is the same as that produced by simple GFAP excess, is not yet clear. Conclusion The implications of these questions for the design of effective treatments are discussed.

scholarly journals Abnormal Reaction to Central Nervous System Injury in Mice Lacking Glial Fibrillary Acidic Protein and Vimentin

1999 ◽  
Vol 145 (3) ◽  
pp. 503-514 ◽  
Author(s):  
Milos Pekny ◽  
Clas B. Johansson ◽  
Camilla Eliasson ◽  
Josefina Stakeberg ◽  
Åsa Wallén ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Glial Fibrillary Acidic Protein ◽  
Intermediate Filament ◽  
Glial Scar ◽  
Scar Formation ◽  
Brain Lesions ◽  
Acidic Protein ◽  
The Central Nervous System

In response to injury of the central nervous system, astrocytes become reactive and express high levels of the intermediate filament (IF) proteins glial fibrillary acidic protein (GFAP), vimentin, and nestin. We have shown that astrocytes in mice deficient for both GFAP and vimentin (GFAP−/−vim−/−) cannot form IFs even when nestin is expressed and are thus devoid of IFs in their reactive state. Here, we have studied the reaction to injury in the central nervous system in GFAP−/−, vimentin−/−, or GFAP−/−vim−/− mice. Glial scar formation appeared normal after spinal cord or brain lesions in GFAP−/− or vimentin−/− mice, but was impaired in GFAP−/−vim−/− mice that developed less dense scars frequently accompanied by bleeding. These results show that GFAP and vimentin are required for proper glial scar formation in the injured central nervous system and that some degree of functional overlap exists between these IF proteins.

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