Details

Autor(en) / Beteiligte

• Milà‐Alomà, Marta
• Salvadó, Gemma
• Gispert, Juan Domingo
• Vilor‐Tejedor, Natalia
• Grau‐Rivera, Oriol
• Sala‐Vila, Aleix
• Sánchez‐Benavides, Gonzalo
• Arenaza‐Urquijo, Eider M.
• Crous‐Bou, Marta
• González‐de‐Echávarri, José Maria
• Minguillon, Carolina
• Fauria, Karine
• Simon, Maryline
• Kollmorgen, Gwendlyn
• Zetterberg, Henrik
• Blennow, Kaj
• Suárez‐Calvet, Marc
• Molinuevo, José Luis

Titel

Amyloid beta, tau, synaptic, neurodegeneration, and glial biomarkers in the preclinical stage of the Alzheimer's continuum

Ist Teil von

• Alzheimer's & dementia, 2020-10, Vol.16 (10), p.1358-1371

Ort / Verlag

Hoboken: John Wiley and Sons Inc

Erscheinungsjahr

2020

Link zum Volltext

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• Introduction The biological pathways involved in the preclinical stage of the Alzheimer's continuum are not well understood. Methods We used NeuroToolKit and Elecsys® immunoassays to measure cerebrospinal fluid (CSF) amyloid‐β (Aβ)42, Aβ40, phosphorylated tau (p‐tau), total tau (t‐tau), neurofilament light (NfL), neurogranin, sTREM2, YKL40, GFAP, IL6, S100, and α‐synuclein in cognitively unimpaired participants of the ALFA+ study, many within the Alzheimer's continuum. Results CSF t‐tau, p‐tau, and neurogranin increase throughout aging only in Aβ‐positive individuals, whereas NfL and glial biomarkers increase with aging regardless of Aβ status. We modelled biomarker changes as a function of CSF Aβ42/40, p‐tau and p‐tau/Aβ42 as proxies of disease progression. The first change observed in the Alzheimer's continuum was a decrease in the CSF Aβ42/40 ratio. This is followed by a steep increase in CSF p‐tau; t‐tau; neurogranin; and, to a lesser extent, in NfL and glial biomarkers. Discussion Multiple biological pathways are altered and could be targeted very early in the Alzheimer's continuum.