Abstract

Objective: We previously reported equivalent sensitivity/specificity when comparing clinical vs. biomarkers to confirm or refute pre-clinical Alzheimer disease (AD) (Wagner, et al., 2012). This case study illustrates the complexity of this combined methodology. Method: A 65-year-old female with a family history of AD presented with a 6 year history of subjective memory loss and fear of AD. Diagnostics were normal including brain MRI with Scheltens 0 for hippocampal atrophy. ADMark, however, showed AB42 719.2 pg/ml, t-tau 587.3 pg/ml, p-tau 86.3 pg/ml and ATI 0.77 which was consistent with AD. There were two neuropsychological studies at year 1 and year 6. Results: Clinical history and objective data showed no significant change over the 5 year observation interval. MMSE remained 30/30. Selective subtests on the WAIS-III/IV were unchanged. Block Design improved 1 scale score (SS) to 11. Digit Span was unchanged at 10. Information was down 2 SS to 12. Coding was up 1 SS to 12. Confrontation naming on BNT was unchanged at T = 57. Trails A & B remained within normal limits. Clock Drawing Test was unchanged at 4/4. WMS showed no change on Logical Memory (LM) I, a 3 SS drop on LM-2 delay to 9, and no change on LM recognition at 27/30. The PAI was abnormal with somatization, anxiety and depression elevated. Conclusion(s): This case illustrates difficulties in clinically defining boundaries of AD when using different markers for early diagnosis and prognostication. The pros and cons were of this combined methodology were discussed.