CSF total and phosphorylated tau protein, regional glucose metabolism and dementia severity in Alzheimer’s disease
C. Haense
Max Planck Institute for Neurological Research, Cologne, Germany
Search for more papers by this authorK. Buerger
Department of Psychiatry, Dementia Research Section and Memory Clinic, Alzheimer Memorial Center and Geriatric Psychiatry Branch, Ludwig-Maximilian University, Munich, Germany
Search for more papers by this authorE. Kalbe
Department of Neurology, University of Cologne, Cologne, Germany
Search for more papers by this authorA. Drzezga
Department of Nuclear Medicine, Technical University Munich, Munich, Germany
Search for more papers by this authorS. J. Teipel
Department of Psychiatry, Dementia Research Section and Memory Clinic, Alzheimer Memorial Center and Geriatric Psychiatry Branch, Ludwig-Maximilian University, Munich, Germany
Department of Psychiatry, University Rostock, Rostock, Germany
Search for more papers by this authorP. Markiewicz
Wolfson Molecular Imaging Centre, University of Manchester, Manchester, UK
Search for more papers by this authorK. Herholz
Department of Neurology, University of Cologne, Cologne, Germany
Wolfson Molecular Imaging Centre, University of Manchester, Manchester, UK
Search for more papers by this authorW. D. Heiss
Max Planck Institute for Neurological Research, Cologne, Germany
Search for more papers by this authorH. Hampel
Department of Psychiatry, Dementia Research Section and Memory Clinic, Alzheimer Memorial Center and Geriatric Psychiatry Branch, Ludwig-Maximilian University, Munich, Germany
Discipline of Psychiatry, School of Medicine and Trinity College Institute of Neuroscience (TCIN), Trinity College Dublin, Trinity Centre for Health Sciences, The Adelaide and Meath Hospital Incorporating the National Children’s Hospital (AMiNCH), Dublin, Ireland
Search for more papers by this authorC. Haense
Max Planck Institute for Neurological Research, Cologne, Germany
Search for more papers by this authorK. Buerger
Department of Psychiatry, Dementia Research Section and Memory Clinic, Alzheimer Memorial Center and Geriatric Psychiatry Branch, Ludwig-Maximilian University, Munich, Germany
Search for more papers by this authorE. Kalbe
Department of Neurology, University of Cologne, Cologne, Germany
Search for more papers by this authorA. Drzezga
Department of Nuclear Medicine, Technical University Munich, Munich, Germany
Search for more papers by this authorS. J. Teipel
Department of Psychiatry, Dementia Research Section and Memory Clinic, Alzheimer Memorial Center and Geriatric Psychiatry Branch, Ludwig-Maximilian University, Munich, Germany
Department of Psychiatry, University Rostock, Rostock, Germany
Search for more papers by this authorP. Markiewicz
Wolfson Molecular Imaging Centre, University of Manchester, Manchester, UK
Search for more papers by this authorK. Herholz
Department of Neurology, University of Cologne, Cologne, Germany
Wolfson Molecular Imaging Centre, University of Manchester, Manchester, UK
Search for more papers by this authorW. D. Heiss
Max Planck Institute for Neurological Research, Cologne, Germany
Search for more papers by this authorH. Hampel
Department of Psychiatry, Dementia Research Section and Memory Clinic, Alzheimer Memorial Center and Geriatric Psychiatry Branch, Ludwig-Maximilian University, Munich, Germany
Discipline of Psychiatry, School of Medicine and Trinity College Institute of Neuroscience (TCIN), Trinity College Dublin, Trinity Centre for Health Sciences, The Adelaide and Meath Hospital Incorporating the National Children’s Hospital (AMiNCH), Dublin, Ireland
Search for more papers by this authorAbstract
Background and purpose: We investigated associations between severity of cognitive impairment, cerebrospinal fluid (CSF) concentrations of total-tau (t-tau) protein and tau phosphorylated at threonin 181 (p-tau181) and regional glucose metabolism measured with 18F-fluorodeoxyglucose-positron emission tomography (18F-FDG-PET) in patients with probable Alzheimer’s disease (AD).
Methods: In 38 patients (mean age 66.5 ± 8.0 years) with AD, Mini-Mental State Examination (MMSE) scores were evaluated and CSF levels of t-tau and p-tau181 measured. All patients underwent an 18F-FDG-PET scan. Image analysis including correlation analysis and principal component analysis (PCA) were performed using SPM5 and VINCI.
Results: Dementia severity (MMSE 21.2 ± 4.9) correlated well with metabolic impairment especially in left hemisphere association areas that are typically affected in patients with AD (e.g. inferior parietal lobule, r = 0.512; medial temporal gyrus, r = 0.478; inferior temporal gyrus, r = 0.488; precuneus, r = 0.468; PCA: r = 0.639, F = 7.751; all P < 0.001). There were no associations between t-tau and p-tau181 with dementia severity and only weak correlations between t-tau and cerebral glucose metabolism (superior parietal gyrus, r = −0.325, P < 0.05; precentral gyrus r = −0.418, P < 0.01; amygdala r = −0.362, P < 0.05). No correlations were found between p-tau181 and regional hypometabolism in FDG-PET.
Conclusion: MMSE and CSF t-tau represent different aspects of disease severity. Whilst MMSE is closely related to impaired cerebral glucose metabolism, CSF t-tau is less closely related and appears to be less well suited for assessment of disease progression.
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