Author(s): Jagust WJ (Jagust, W. J.); Landau SM (Landau, S. M.); Shaw LM (Shaw, L. M.); Trojanowski JQ (Trojanowski, J. Q.); Koeppe RA (Koeppe, R. A.); Reiman EM (Reiman, E. M.); Foster NL (Foster, N. L.); Petersen RC (Petersen, R. C.); Weiner MW (Weiner, M. W.); Price JC (Price, J. C.); Mathis CA (Mathis, C. A.)

Title: Relationships between biomarkers in aging and dementia

Source: NEUROLOGY 73 (15): 1193-1199

Date: 2009 OCT 13

Document Type: Journal : Article

DOI: 10.1212/WNL.0b013e3181bc010c

Language: English

LCR: 1   CR: 31   LCS: 4   GCS: 23   SCS: 

Comment:  

Address: [Jagust, W. J.; Landau, S. M.] Univ Calif Berkeley, Helen Wills Neurosci Inst, Berkeley, CA 94620 USA.
[Jagust, W. J.; Landau, S. M.] Univ Calif Berkeley, Lawrence Berkeley Lab, Berkeley, CA 94620 USA.
[Shaw, L. M.; Trojanowski, J. Q.] Univ Penn, Sch Med, Dept Pathol & Lab Med, Inst Aging,Ctr Neurodegenerat Dis Res, Philadelphia, PA 19104 USA.
[Koeppe, R. A.] Univ Michigan, Dept Radiol, Div Nucl Med, Ann Arbor, MI 48109 USA.
[Reiman, E. M.] Banner Alzheimers Inst, Phoenix, AZ USA.
[Reiman, E. M.] Banner Good Samaritan PET Ctr, Phoenix, AZ USA.
[Foster, N. L.] Univ Utah, Ctr Alzheimers Care Imaging & Res, Salt Lake City, UT USA.
[Foster, N. L.] Univ Utah, Dept Neurol, Salt Lake City, UT USA.
[Petersen, R. C.] Mayo Clin, Dept Neurol, Coll Med, Rochester, MN USA.
[Weiner, M. W.] Ctr Imaging Neurodegenerat Dis, Dept Vet Affairs Med Ctr, San Francisco, CA USA.
[Price, J. C.; Mathis, C. A.] Univ Pittsburgh, Dept Radiol, Pittsburgh, PA 15260 USA.

Reprint: Jagust, WJ, Univ Calif Berkeley, Helen Wills Neurosci Inst, 132 Barker
Hall, Berkeley, CA 94620 USA.

E-mail: jagust@berkeley.edu

Author Keywords:  

KeyWords Plus: MILD COGNITIVE IMPAIRMENT; POSITRON-EMISSION-TOMOGRAPHY; PHOSPHORYLATED TAU-PROTEIN; PITTSBURGH COMPOUND-B; ALZHEIMERS-DISEASE; CEREBROSPINAL-FLUID; AMYLOID DEPOSITION; CLINICAL-DIAGNOSIS; GLUCOSE-METABOLISM; PET

Abstract: Background: PET imaging using [F-18]fluorodeoxyglucose (FDG) and [C-11]Pittsburgh compound B (PIB) have been proposed as biomarkers of Alzheimer disease (AD), as have CSF measures of the 42 amino acid beta-amyloid protein (A beta(1-42)) and total and phosphorylated tau (t-tau and p-tau). Relationships between biomarkers and with disease severity are incompletely understood. Methods: Ten subjects with AD, 11 control subjects, and 34 subjects with mild cognitive impairment from the Alzheimer's Disease Neuroimaging Initiative underwent clinical evaluation; CSF measurement of A beta(1-42), t-tau, and p-tau; and PIB-PET and FDG-PET scanning. Data were analyzed using continuous regression and dichotomous outcomes with subjects classified as "positive" or "negative" for AD based on cutoffs established in patients with AD and controls from other cohorts. Results: Dichotomous categorization showed substantial agreement between PIB-PET and CSF A beta(1-42) measures (91% agreement, kappa = 0.74), modest agreement between PIB-PET and p-tau (76% agreement, kappa = 0.50), and minimal agreement for other comparisons (kappa < 0.3). Mini-Mental State Examination score was significantly correlated with FDG-PET but not with PIB-PET or CSF A beta(1-42). Regression models adjusted for diagnosis showed that PIB-PET was significantly correlated with A beta(1-42), t-tau, and p-tau(181p), whereas FDG-PET was correlated only with A beta(1-42). Conclusions: PET and CSF biomarkers of A beta agree with one another but are not related to cognitive impairment. [F-18]fluorodeoxyglucose-PET is modestly related to other biomarkers but is better related to cognition. Different biomarkers for Alzheimer disease provide different information from one another that is likely to be complementary. Neurology (R) 2009; 73: 1193-1199