Aktuelle Neurologie 2009; 36 - V285
DOI: 10.1055/s-0029-1238452

CSF Tau, phospho-Tau181 and amyloid-β 38/40/42 in frontotemporal dementia and pimary progressive aphasia

A Hofmann 1, V Welge 1, O Fiege 1, P Lewczuk 1, S Wolf 1, B Mollenhauer 1, J Wiltfang 1, M Bibl 1
  • 1Essen, Erlangen, Göttingen, Kassel

Over the past ten years, characteristic cerebrospinal fluid (CSF) biomarker patterns have been established for supporting the clinical diagnosis of Alzheimer's dementia (AD). In contrast, the literature about specific biomarkers for other frequent neurodegenerative dementias is sparser. Aside frontotemporal dementia (FTD) primary progressive aphasia (PPA) represents a major group among frontotemporal lobe degenerations (FTLD). This prompted us to determine the major amyloid-β (A-β) species in CSF 1–40, 1–38 and 1–42 in addition to total tau and p-tau181 in patients with FTD (n=25) and PPA (n=12), respectively, as compared to AD (n=25) and non demented disease controls (NDC, n=20) by electrochemiluminescence and ELISA, respectively.

FTD displayed lower overall A-β levels (p=1.5×10-3), pronouncedly of A-β 1–38 (p=4.1×10-4) and higher levels of p-tau (p=5.3×10-3) than NDC. In comparison to AD, there were lower levels of A-β1–38 (p=1.9×10-5), A-β 1–40 (p=4.5×10-3), p-tau (p=4.2×10-9) and tau (p=6.3×10-6) accompanied by higher levels of A-β 1–42 (p=8.7×10-7).

PPA displayed lower overall A-β levels (p=4.5×10-2) and a tendency to lower levels of A-β 1–40 and A-β 1–42 than NDC, which failed the level of significance. Other parameters were unaltered. In comparison to AD, there were lower levels of p-tau (p=6.2×10-6) as well as a tendency to lower tau and A-β1–38 levels, which failed the level of significance. A-β 1–42 levels were lower in AD (p=2×10-4).

As compared to FTD, PPA showed higher levels of p-tau (p=1.8×10-2), tau (p=14×10-2) and A-β 1–38 (p=1.6×10-2). A-β 1–40 and A-β 1–42 were unaltered between these groups.

There was no significant difference between NDC subgroups (depressive cognitive complainers (DCC, n=10), peripheral neurological diseases (PND, n=10).

In conclusion there are distinct patterns of dementia biomarkers among the two clinical subgroups of FTLD FTD and PPA. Further studies will have to clarify the diagnostic value of subclassification of dementias other than AD by CSF based biomarkers. For the lack of neuropathological characterization of our patient groups, the pathophysiological background of our findings remain obscure.