Amyloid β(1-42) and phosphorylated tau in CSF as markers for early-onset Alzheimer disease

N. S.M. Schoonenboom*, Y. A.L. Pijnenburg, C. Mulder, S. M. Rosso, E. J. Van Elk, G. J. Van Kamp, J. C. Van Swieten, Ph Scheltens

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review


Objective: To determine the diagnostic value of CSF amyloid β(1-42) (Aβ42), 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 Aβ42, 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 Aβ42 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 Aβ42 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 Aβ42 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 Aβ42 and CSF Ptau-181 may help in differentiating EAD from FTLD.

Original languageEnglish
Pages (from-to)1580-1584
Number of pages5
Issue number9
Publication statusPublished - 11 May 2004

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