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

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.

2004 ◽  
Vol 67 (5) ◽  
pp. 1050-1052 ◽  
Author(s):  
R. R. COORE ◽  
S. LOVE ◽  
J. L. McKINSTRY ◽  
H. R. WEAVER ◽  
A. PHILLIPS ◽  
...  

The epidemic of bovine spongiform encephalopathyin the United Kingdom and the recognition of a variant of Creutzfeldt-Jakob disease prompted revision of the guidelines for slaughter of cattle and sheep to prevent contamination of the edible parts of the carcass with central nervous system tissue. We previously showed that captive bolt gun stunning, which is routinely used for the slaughter of cattle and sheep, causes entry of fragments of central nervous system tissue into the jugular vein. To determine whether such tissue can traverse pulmonary capillaries to enter the systemic circulation, we introduced small volumes of brain tissue that had been disrupted by stunning with a captive bolt gun into the jugular vein of sheep sent for slaughter. We examined aortic blood samples by immunocytochemistry for neurofilament and S100 proteins and by enzyme-linked immunosorbent assay for glial fibrillary acidic protein and found fragments of neurofilament- and S100-immunopositive central nervous system tissue in samples from 2 of 11 sheep and elevated glial fibrillary acidic protein in 6 sheep. Our findings suggest that central nervous system tissue that is dislodged during routine captive bolt gun stunning and slaughter of sheep can enter the systemic arterial circulation and that, in some cases, this method of slaughter of an animal infected with bovine spongiform encephalopathy would be likely to contaminate edible parts of the carcass with infective material.


Author(s):  
Albee Messing

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.


1999 ◽  
Vol 145 (3) ◽  
pp. 503-514 ◽  
Author(s):  
Milos Pekny ◽  
Clas B. Johansson ◽  
Camilla Eliasson ◽  
Josefina Stakeberg ◽  
Åsa Wallén ◽  
...  

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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