Cerebral changes and cerebrospinal fluid β-amyloid in Alzheimer's disease

• Verfasst von: Schröder, Johannes [VerfasserIn]
• Verfasst von: Pantel, Johannes [VerfasserIn]
• Verfasst von: Ida, N. [VerfasserIn]
• Verfasst von: Essig, Marco [VerfasserIn]
• Verfasst von: Hartmann, Tobias [VerfasserIn]
• Verfasst von: Knopp, Michael V. [VerfasserIn]
• Verfasst von: Schad, Lothar R. [VerfasserIn]
• Verfasst von: Sandbrink, Rupert [VerfasserIn]
• Verfasst von: Sauer, H. [VerfasserIn]
• Verfasst von: Masters, C. L. [VerfasserIn]
• Verfasst von: Beyreuther, Konrad [VerfasserIn]
• Titel: Cerebral changes and cerebrospinal fluid β-amyloid in Alzheimer's disease
• Titelzusatz: a study with quantitative magnetic resonance imaging
• Verf.angabe: J. Schröder, J. Pantel, N. Ida, M. Essig, T. Hartmann, M.V. Knopp, L.R. Schad, R. Sandbrink, H. Sauer, C.L. Masters, K. Beyreuther
• E-Jahr: 1997
• Jahr: 01 October 1997
• Umfang: 3 S.
• Fussnoten: Gesehen am 16.11.2021
• Titel Quelle: Enthalten in: Molecular psychiatry
• Ort Quelle: [London] : Springer Nature, 1997
• Jahr Quelle: 1997
• Band/Heft Quelle: 2(1997), 6, Seite 505-507
• ISSN Quelle: 1476-5578
• DOI: doi:10.1038/sj.mp.4000313
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: Behavioral Sciences
• Sach-SW: Biological Psychology
• Sach-SW: general
• Sach-SW: Medicine/Public Health
• Sach-SW: Neurosciences
• Sach-SW: Pharmacotherapy
• Sach-SW: Psychiatry
• K10plus-PPN: 1777521580

Abstract

Pathological and biochemical studies indicate that β-amyloid (βA4) deposition is a hallmark in the pathogenesis of Alzheimer's disease (AD).1-4 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).5,6 Therefore one may expect that reduced βA4-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 β A4 and its major C-terminal variations β A4 1-40 and β A4 1-42 were compared with cerebral changes as assessed by quantitative magnetic resonance imaging (MRI). Significantly (P < 0.05) reduced β A4 1-40 and β A4 1-42 levels were found in the AD patients (17 female; six male; AD/NINCDS-ADRDA-criteria)7 in comparison to the patients with major depression (seven female; two male; DSM-III-R).8 Within the AD group, βA4 and β xA4 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 β A4 levels contribute to temporal lobe atrophy in AD and support the possibility that βA4 is central to the etiology of AD.