Abstract
We have measured plasma progranulin and interleukin-6 in 230 patients with frontotemporal lobar degeneration (FTLD), 104 patients with Alzheimer's disease, and 161 control subjects. We have replicated previous findings of decreased levels of progranulin protein in FTLD because of mutations in GRN and show this is not observed in FTLD cases because of other causes. interleukin-6 levels were increased in FTLD overall, but these did not discriminate between clinical and genetic subtypes.
Highlights
We have measured plasma progranulin and interleukin-6 in 230 patients with frontotemporal lobar degeneration (FTLD), 104 patients with Alzheimer’s disease, and 161 control subjects
We have replicated previous findings of decreased levels of progranulin protein in FTLD because of mutations in GRN and show this is not observed in FTLD cases because of other causes. interleukin-6 levels were increased in FTLD overall, but these did not discriminate between clinical and genetic subtypes
We measured plasma PGRN and interleukin-6 (IL-6) in patients with FTLD, Alzheimer’s disease (AD), and healthy control subjects to ascertain whether levels of these have potential to discriminate patients with FTLD from other neurodegenerative disorders (AD) and healthy individuals, and whether they can differentiate between clinical, neurohistologic, and genetic subtypes of FTLD
Summary
We have measured plasma progranulin and interleukin-6 in 230 patients with frontotemporal lobar degeneration (FTLD), 104 patients with Alzheimer’s disease, and 161 control subjects. Analysis of variance was used to compare age at onset, age at sampling, duration of illness, PGRN and IL-6 levels between the various clinical diagnostic and genetic groups with post hoc testing (subject to Bonferroni correction) when a significantly different analysis of variance result was obtained.
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