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NEUROLOGY 2008;70:1827-1835
© 2008 American Academy of Neurology

CSF biomarkers in frontotemporal lobar degeneration with known pathology

H. Bian, MD, J. C. Van Swieten, MD, S. Leight, BA, L. Massimo, LPN, E. Wood, MS, M. Forman, MD, PhD, P. Moore, BA, I. de Koning, PhD, C. M. Clark, MD, S. Rosso, MD, J. Trojanowski, MD, PhD, V. M.-Y. Lee, PhD and M. Grossman, MD

From the Department of Neurology (H.B., L.M., P.M., C.M.C., M.G.), Department of Pathology and Laboratory Medicine (S.L., E.W., M.F., J.T., V.M.-Y.L.), Center for Neurodegenerative Disease Research (S.L., E.W., M.F., J.T., V.M.-Y.L.), Institute on Aging (S.L., J.T., V.M.-Y.L.), and Alzheimer’s Disease Center (C.M.C.), University of Pennsylvania School of Medicine, Philadelphia; Department of Neurology, Erasmus University Medical Centre (J.C.V.S., I.d.k., S.R.), Rotterdam, Netherlands; and Department of Neurology, Jinan Central Hospital, Shandong University School of Medicine (H.B.), Jinan, Shandong Province, People’s Republic of China.

Address correspondence and reprint requests to Dr. Murray Grossman, Department of Neurology, 2 Gibson, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA 19104-4283 mgrossma{at}mail.med.upenn.edu

Objective: To evaluate the diagnostic value of CSF biomarkers in patients with known pathology due to frontotemporal lobar degeneration (FTLD).

Background: It is important to distinguish FTLD from other neurodegenerative diseases like Alzheimer disease (AD), but this may be difficult clinically because of atypical presentations.

Methods: Patients with FTLD (n = 30) and AD (n = 19) were identified at autopsy or on the basis of genetic testing at University of Pennsylvania and Erasmus University Medical Center. CSF was obtained during a diagnostic lumbar puncture and was analyzed using assays for total tau and amyloid-beta 1-42 (Aβ42). Patients also were assessed with a brief neuropsychological battery.

Results: CSF total tau level and the ratio of CSF total tau to Aβ42 (tau/Aβ42) were significantly lower in FTLD than in AD. Receiver operating characteristic curve analyses confirmed that the CSF tau/Aβ42 ratio is sensitive and specific at discriminating between FTLD and AD, and is more successful at this than CSF total tau alone. Although some neuropsychological measures are significantly different in autopsy-proven FTLD and AD, combining these neuropsychological measures with CSF biomarkers did not improve the ability to distinguish FTLD from AD.

Conclusions: The ratio of CSF tau/Aβ42 is a sensitive and specific biomarker at discriminating frontotemporal lobar degeneration from Alzheimer disease in patients with known pathology.

Abbreviations: AD = Alzheimer disease; AUC = area under the curve; CBD = corticobasal degeneration; FTLD = frontotemporal lobar degeneration; FTLD-U = FTLD with ubiquitin-positive but tau-negative inclusions; MAPT = microtubule-associated protein tau; MND = motor neuron disease; PiD = dementia with Pick bodies; ROC = receiver operating characteristic; TPSD = tangle predominant senile dementia.

Supported in part by NIH (AG17586, AG15116, and NS44266) and the Dana Foundation.

Disclosure: The authors report no conflicts of interest.

Received June 7, 2007. Accepted in final form August 31, 2007.






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