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I appreciate that Frisoni and colleagues took our previous results, placed them into a clinical context, and concluded that detection of the biological fingerprint of AD in patients with MCI might be sufficiently accurate for clinical decisions.

In our exploratory study, we identified elevated tau protein and decreased A42 protein concentrations at baseline in the CSF of patients with MCI who subsequently progressed to AD, yielding sensitivity and specificity values of 90% each. We also observed elevated CSF tau protein concentrations in subjects with MCI who showed a worsening of cognitive symptoms that was not severe enough to fulfill the diagnostic criteria of AD. Logistic regression analysis identified tau as the only variable among several others that predicted the progression of clinical symptoms. Therefore, elevated tau protein in CSF as a marker of neuronal degeneration and to a lesser extent decreased A42 protein may be the . . . [Full Text of this Article]

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