University of Heidelberg
Faculty of Medicine Mannheim
University Hospital Mannheim
These pages are still under constructions and will be available soon! Please check again later!

If you have questions concerning a specific publication please use this form with subject 'information about publications' and giving the full citation in the message body.

Collaborate Research Projects
Home > Publications > Abstract >

Cerebral changes and cerebrospinal fluid beta-amyloid in Alzheimer's disease: a study with quantitative magnetic resonance imaging

J. Schröder, J. Pantel, N. Ida, M. Essig, T. Hartmann, M. Knopp, L. Schad, R. Sandbrink, H. Sauer, C. Masters and K. Beyreuther

Mol Psychiatry, 2 (6), pp.505-507

Pathological and biochemical studies indicate that beta-amyloid (betaA4) deposition is a hallmark in the pathogenesis of Alzheimer's disease (AD). Neuroimaging studies demonstrate that the respective cerebral changes primarily strike the temporal lobe and the amygdala-hippocampus complex and may be reliably assessed using quantitative magnetic resonance imaging (MRI). Therefore one may expect that reduced betaA4-levels are significantly correlated with measures of the temporal lobe rather than global cerebral atrophy in AD patients. To test this hypothesis in a clinical study, cerebrospinal fluid concentrations of total betaA4 and its major C-terminal variations betaA4 1-40 and betaA4 1-42 were compared with cerebral changes as assessed by quantitative magnetic resonance imaging (MRI). Significantly (P< 0.05) reduced betaA4 1-40 and betaA4 1-42 levels were found in the AD patients (17 female; six male; AD/NINCDS-ADRDA-criteria) in comparison to the patients with major depression (seven female; two male; DSM-III-R). Within the AD group, betaA4 and betaA4 1-42 levels were significantly correlated with the volume of the temporal lobes (r= 0.46 and r= 0.48, respectively) but none of the other volumetric measures. These findings indicate that changes in cerebral betaA4 levels contribute to temporal lobe atrophy in AD and support the possibility that betaA4 is central to the etiology of AD.

Contact: Dr. Frank Zöllner last modified: 30.09.2020
to top of page