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Letter to the editor

In a recent paper, Ågren-Wilsson et al. (1) reported elevated CNS concentrations of NFL in idiopathic normal pressure hydrocephalus (INPH) and subcortical arteriosclerotic encephalopathy (SAE), while levels of total tau (T-tau), phosphorylated tau (P-tau) and Ab-42 were lower in INPH compared with those in SAE and controls. These data suggest the power of the combination of NFL, P-tau and Ab-42 in distinguishing between the clinical diagnoses of INPH, SAE and healthy controls. Unfortunately, the authors did not mention previous studies by Lins et al. (2) who measured T-tau and Ab-42 in patients with INPH, SAE, AD and Parkinson s disease (PD) without dementia (n = 12 each), and 24 nondemented, age-matched controls, using specific ELISA methods. T-tau in INPH was not significantly different from SAE, PD and controls, while Ab-42 in INPH was significantly decreased compared with that in PD, SAE and controls, AD, a significant increase in T-tau and a significant decrease in Ab-42 were seen, the latter findings being in concordance with many other studies. Using a relation between T-tau and Ab-42, all cases of INPH, SAE and controls were within the non-AD plot region, while 92% each of AD and SAE samples were within the AD and non-AD area respectively. Without using P-tau at that time, the authors concluded that the combined measurement of T-tau and Ab-42 in CSF alone appears adequate to differentiate INPH as well as PD and non-demented controls from AD, and SAE vs. AD respectively.