Reduced CSF carboxyterminally truncated A beta peptides in frontotemporal lobe degenerations

2007 | journal article. A publication with affiliation to the University of Göttingen.

Jump to: Cite & Linked | Documents & Media | Details | Version history

Cite this publication

​Reduced CSF carboxyterminally truncated A beta peptides in frontotemporal lobe degenerations​
Bibl, M.; Mollenhauer, B.; Wolf, S.; Esselmann, H.; Lewczuk, P.; Kornhuber, J. & Wiltfang, J.​ (2007) 
Journal of Neural Transmission114(5) pp. 621​-628​.​ DOI: https://doi.org/10.1007/s00702-006-0618-z 

Documents & Media

License

GRO License GRO License

Details

Authors
Bibl, Mirko; Mollenhauer, Brit; Wolf, S.; Esselmann, Herrmann; Lewczuk, Piotr; Kornhuber, Johannes; Wiltfang, J.
Abstract
Cerebrospinal fluid (CSF) carboxyterminally truncated amyloid-beta (A beta) peptides, A beta 1-42 and tau protein were evaluated in 30 patients with frontotemporal lobe degenerations (FTLD), 30 Alzheimer's disease (AD) patients and 30 non-demented disease controls (NDC) by A beta-SDS-PAGE/immunoblot as well as commercial ELISAs for A beta 1-42 and total tau. FTLD displayed a significant drop of A beta 1-37 (p = 2.7 x 10(-4)), A beta 1-38 (p = 4.2 x 10(-5)) and A beta 1-42 (p = 3.3 x 10(-4)). A beta 1-42 was selectively decreased in AD (p = 8.5 x 10(-1)). Decreased A beta 1-38 enabled contrasts of beyond 85% to distinguish FTLD from AD and NDC patients, alone or in combination. Accordingly, low CSF A beta 1-37 and A beta 1-38 represent a biomarker candidate for FTLD and may reflect disease-specific changes of APP metabolism. Further validation should be carried out on dementias other than AD, diagnostically relevant control groups without dementia and without any evident affection of the central nervous system and subgroups of FTLD. Moreover, independent methods of measurement should be applied to CSF A beta 1-38.
Issue Date
2007
Status
published
Publisher
Springer
Journal
Journal of Neural Transmission 
ISSN
0300-9564

Reference

Citations


Social Media