Publication Detail
The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Demonstration of a novel neurofilament associated antigen with the neurofibrillary pathology of Alzheimer and related diseases.
J Gheuens; P Cras; G Perry; J Boons; C Ceuterick-de Groote; U Lübke; M Mercken; M Tabaton; P L Gambetti; M Vandermeeren (Profiled Author: Perry, George)
Laboratory of Neuropathology, Born Bunge Foundation, University of Antwerp, Wilrijk, Belgium.
Brain research 1991;558(1):43-52.
A monoclonal antibody, termed NFT200, was raised after in vitro immunization with sonicated neurofibrillary tangle (NFT)-enriched fractions prepared from Alzheimer brain. The antigen to which NFT200 is directed was expressed in the paired helical filaments of NFT in sporadic and familial Alzheimer disease (AD), in the straight filaments of NFT in AD, progressive supranuclear palsy and of Pick bodies, and the NFT in several other conditions such as Parkinson-dementia complex of Guam and subacute sclerosing panencephalitis. Granulovacuolar degeneration of AD was also labeled with NFT200. Hirano bodies and amyloid deposits in AD, as well as Lewy bodies of idiopathic Parkinson disease lacked in the antigen. The NFT200-antigen was also expressed as a phosphatase-insensitive antigen in normal neurofilaments found in spinal cord and peripheral nerve axons but was absent from the perikaryal accumulation of neurofilaments induced by aluminum intoxication. Nevertheless, immunoblot studies failed to detect the NFT200 in isolated preparations of the neurofilament proteins, MAP-2, tau, ubiquitin or A4-amyloid peptide. The results indicate that the NFT200 monoclonal antibody is directed against a phosphatase-insensitive epitope of an axonal protein associated with neurofilaments but is labile to isolation and expressed as a stable epitope of a 200 kDa component of NFT.
2 Originating Grant
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1.
PERRY, GEORGE
NEUROFIBRILLARY PATHOLOGY IN ALZHEIMER DISEASE
1 September 1990 - 30 November 2000
NATIONAL INSTITUTE ON AGING
Total Funding: $ 1,191,333
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2.
PERRY, GEORGE
AMYLOID PRECURSOR IN ALZHEIMERS DISEASE
1 April 1988 - 30 June 1995
NATIONAL INSTITUTE ON AGING
Total Funding: $ 536,600
Scientific Context
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
Related Grants
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1.
RAPOPORT, STANLEY I
NATIONAL INSTITUTE ON AGING
Total Funding: $ 1,242,387
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2.
SELKOE, DENNIS J
MOLECULAR PATHOLOGY OF ALZHEIMER PAIRED HELICAL FILAMENT
1 May 1987 - 31 October 1989
NATIONAL INSTITUTE ON AGING
Total Funding: $ 260,772
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3.
SELKOE, DENNIS J
MOLECULAR PATHOLOGY OF ALZHEIMER PAIRED HELICAL FILAMENT
1 June 1985 - 30 November 1986
NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE
Total Funding: $ 161,851
Related Publications
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1.
1987D W Dickson; H Ksiezak-Reding; P Davies; S H Yen
Acta neuropathologica 1987;73(3):254-8. -
2.
1987C L Joachim; J H Morris; D J Selkoe; K S Kosik
Tau epitopes are incorporated into a range of lesions in Alzheimer's disease.
Journal of neuropathology and experimental neurology 1987;46(6):611-22. -
3.
1986G Perry; D J Selkoe; B R Block; D Stewart; L Autilio-Gambetti; P Gambetti
Journal of neuropathology and experimental neurology 1986;45(2):161-8.
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