-
Neuropsychiatric Disease and Treatment
-
About Dovepress
Open access peer-reviewed scientific and medical journals.
-
Open Access
Dove Medical Press is now a member of the Open Access Initiative
-
An Author's Guide
A guide to help authors get their paper published.
-
Advocacy
Support Open Access and Dove Press
-
Reprints
Promotional Article Monitoring - further details
-
Favored Author Program
Real benefits for authors, including fast-track processing of papers.
CSF tau protein and FDG PET in patients with aging-associated cognitive decline and Alzheimer’s disease
(1764) Views (265) Full article downloads
Authors: Aoife Hunt, Peter Schönknecht, Markus Henze, Pablo Toro, Uwe Haberkorn, Johannes Schröder
Published Date February 2006
Volume 2006:2(2) Pages 207 - 212
DOI: http://dx.doi.org/10.2147/NDT.S
Aoife Hunt, Peter Schönknecht, Markus Henze, Pablo Toro, Uwe Haberkorn, Johannes Schröder
Memory Clinic, Section of Geriatric Psychiatry, University Hospital Heidelberg, Ruprecht-Karls-University, Germany
Introduction: In Alzheimer’s disease (AD), accelerated neurofibrillary tangle formation occurs which is associated with increased tau protein release into the cerebrospinal fluid (CSF). Recent studies found significantly increased CSF tau already in patients at risk of developing AD, indicating its potential as a biochemical marker of AD. Cerebral glucose metabolism is reduced in frontotemporoparietal and cingulate cortices in patients with mild AD. However, few studies have investigated CSF tau protein and cerebral glucose metabolism changes in patients at risk to develop AD.
Methods: 48 patients with AD, 88 patients with aging-associated cognitive decline (AACD), and 39 healthy controls were included. In all participants, CSF levels of tau were determined by ELISA at baseline and compared between the diagnostic groups. 14 AACD patients and 14 controls underwent 18F-fluorodeoxyglucose positron emission tomography (FDG PET).
Results: AD patients showed the highest CSF tau levels compared with AACD patients and controls. AACD patients had significantly higher tau levels than the controls but lower than the AD patients. AACD patients were characterized by reduced glucose metabolism in bilateral middle temporal cortex, left posterior cingulate cortex, right angular gyrus, and right precuneus compared with controls.
Conclusion: In conclusion, our findings reflect and confirm the clinical judgment of an incipient neurodegenerative disorder in a considerable portion of AACD patients. In patients with AACD, CSF tau levels and cerebral glucose metabolism show an altered pattern comparable with that found in AD and thus may facilitate early diagnosis.
Keywords: Aging-associated cognitive decline, Alzheimer’s disease, CSF tau protein, FDG PET
Readers of this article also read:
Risperidone in the treatment of bipolar mania
The use of atypical antipsychotics beyond psychoses: efficacy of quetiapine in bipolar disorder
Bipolar disorders: treatment options and patient satisfaction
Restless legs syndrome: diagnosis and review of management options
- Have an opinion about one of our articles?
We encourage you to write a Letter to the Editor
- Journal Indexing
See where all the Dove Press journals are indexed
- Testimonials
"... I was impressed at the rapidity of publication from submission to final acceptance." Dr Edwin Thrower, PhD, Yale University
- Long-term treatment of bipolar disorder with a radioelectric asymmetric conveyor
- Implementing the 2009 Institute of Medicine recommendations on resident physician work hours, supervision, and safety
- Moderate alcohol consumption and cognitive risk
- Topiramate in the prevention and treatment of migraine: efficacy, safety and patient preference




