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From the Alzheimer Center (Drs. Schoonenboom, Pijnenburg, and Scheltens), Department of Neurology, and Department of Clinical Chemistry (Drs. Schoonenboom and Van Kamp, C. Mulder and E.-J. Van Elk), VU University Medical Center, Amsterdam, and Department of Neurology (Drs. Rosso and Van Swieten), Erasmus Medical Center, Rotterdam, the Netherlands.
Address correspondence and reprint requests to Dr. N.S.M. Schoonenboom, Alzheimer Center, Department of Neurology, VU University Medical Center, PO Box 7057, 1007 MB Amsterdam, the Netherlands; e-mail: niki.schoonenboom{at}vumc.nl
Objective: To determine the diagnostic value of CSF amyloid ß(1–42) (Aß42), CSF total tau, and CSF tau phosphorylated at threonine-181 (Ptau-181) in early-onset Alzheimer disease (EAD) vs frontotemporal lobar degeneration (FTLD).
Methods: Levels of Aß42, total tau, and Ptau-181 in CSF were measured using commercially available ELISA in 47 EAD patients, 28 FTLD patients, and 21 nondemented control subjects.
Results: CSF Aß42 was significantly lower and CSF total tau and CSF Ptau-181 significantly higher in EAD patients than FTLD patients and control subjects. There was an increase in diagnostic accuracy for CSF Ptau-181 vs CSF total tau (p = 0.067). Combining low CSF Aß42 and high CSF Ptau-181 allowed EAD patients to be distinguished from FTLD patients with a sensitivity of 72% and a specificity of 93%. Logistic regression analysis with CSF Aß42 and CSF Ptau-181 as independent continuous variables resulted in correct classification of 46 of 47 (98%) EAD patients and 23 of 28 (82%) FTLD patients. The diagnostic accuracy for EAD was independent of gender, disease duration, and disease severity.
Conclusion: The combination of CSF Aß42 and CSF Ptau-181 may help in differentiating EAD from FTLD.
Received July 22, 2003. Accepted in final form January 9, 2004.
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