1. Different CSF β-amyloid processing in Alzheimer's and Creutzfeldt-Jakob disease.
- Author
-
Mollenhauer B, Esselmann H, Roeber S, Schulz-Schaeffer WJ, Trenkwalder C, Bibl M, Steinacker P, Kretzschmar HA, Wiltfang J, and Otto M
- Subjects
- Adult, Aged, Aged, 80 and over, Alzheimer Disease pathology, Brain metabolism, Creutzfeldt-Jakob Syndrome pathology, Female, Humans, Immunoprecipitation methods, Male, Middle Aged, Alzheimer Disease cerebrospinal fluid, Amyloid beta-Peptides cerebrospinal fluid, Creutzfeldt-Jakob Syndrome cerebrospinal fluid, Peptide Fragments cerebrospinal fluid
- Abstract
Decreased levels of β-amyloid (Aβ) 1-42 in cerebrospinal fluid (CSF) are characteristic for Alzheimer's disease (AD) and are also evident in Creutzfeldt-Jakob disease (CJD). Aβ plaques are thought to be responsible for this decrease in AD patients, whereas such Aβ plaques are rarely seen in CJD. To investigate the Aβ pattern in brain and CSF of neuropathologically confirmed CJD and AD patients we used an electrophoretic method to investigate Aβ peptide fractions which are not accessible to ELISA and immunohistochemistry. We analyzed Aβ peptides in the CSF of autopsy-confirmed CJD and AD patients and the corresponding brain homogenates using a quantitative urea-based Aβ electrophoresis immunoblot (Aβ-SDS-PAGE/immunoblot).The CSF Aβ1-42 decrease correlated with the brain Aβ load in AD, but not in CJD. There was no difference in the soluble fractions of brain homogenate in AD and CJD. We therefore conclude that different mechanisms in AD and CJD are responsible for the Aβ1-42 decrease in the CSF.
- Published
- 2011
- Full Text
- View/download PDF