PMC:4845325 / 6741-7610 JSONTXT

{"project":"2_test","denotations":[{"id":"27112350-17569065-72613473","span":{"begin":554,"end":555},"obj":"17569065"},{"id":"27112350-19805492-72613473","span":{"begin":554,"end":555},"obj":"19805492"},{"id":"27112350-23543794-72613473","span":{"begin":554,"end":555},"obj":"23543794"},{"id":"27112350-24656258-72613474","span":{"begin":744,"end":745},"obj":"24656258"}],"text":"To determine to what extent the observed changes in the AD signaling proteome are AD specific or the result of general neurodegeneration or other unrelated processes, we collected plasma samples from an additional 92 patients (Additional file 1: Table S2) suffering from semantic-variant primary progressive aphasia (svPPA), a sub-type of frontotemporal lobar degeneration (FTLD). SvPPA is almost always associated with Trans-activation response element (TAR) DNA-binding protein 43 (TDP-43)-aggregate pathology and appears to have weak genetic linkage [5–7]. This makes svPPA an ideal candidate to compare distinct neurological pathologies between two unrelated, sporadic, progressive dementias (svPPA vs. AD) via signaling proteome analysis [8]. The svPPA samples were prepared, handled, and analyzed in parallel to the AD samples to minimize experimental variations."}