<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Cacciaglia R</submitter><funding>European Research Council</funding><funding>NIA NIH HHS</funding><pagination>fcae451</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11668178</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>7(1)</volume><pubmed_abstract>CSF concentrations of β-amyloid 42 (Aβ42) and phosphorylated tau (p-tau) are well-established biomarkers of Alzheimer's disease and have been studied in relation to several neuropathological features both in patients and in cognitively unimpaired individuals. The CSF p-tau/Aβ42 ratio, a biomarker combining information from both pathophysiological processes, has emerged as a promising tool for monitoring disease progression, even at pre-clinical stages. Here, we studied the association between the CSF p-tau/Aβ42 ratio with downstream markers of pre-clinical Alzheimer's disease progression including brain structure, glucose metabolism, fibrillary Aβ deposition and cognitive performance in 234 cognitively unimpaired individuals, who underwent cognitive testing, a lumbar puncture, MRI, 18F-flu</pubmed_abstract><journal>Brain communications</journal><pubmed_title>The CSF p-tau/β-amyloid 42 ratio correlates with brain structure and fibrillary β-amyloid deposition in cognitively unimpaired individuals at the earliest stages of pre-clinical Alzheimer's disease.</pubmed_title><pmcid>PMC11668178</pmcid><funding_grant_id>948677</funding_grant_id><funding_grant_id>R01 AG068398</funding_grant_id><pubmed_authors>Canas A</pubmed_authors><pubmed_authors>Suarez-Calvet M</pubmed_authors><pubmed_authors>Gil CM</pubmed_authors><pubmed_authors>Gamez LI</pubmed_authors><pubmed_authors>Radoi IA</pubmed_authors><pubmed_authors>Rodriguez GH</pubmed_authors><pubmed_authors>Huguet J</pubmed_authors><pubmed_authors>Soteras A</pubmed_authors><pubmed_authors>Zetterberg H</pubmed_authors><pubmed_authors>Stankeviciute LS</pubmed_authors><pubmed_authors>Grau-Rivera O</pubmed_authors><pubmed_authors>Gispert JD</pubmed_authors><pubmed_authors>Falcon C</pubmed_authors><pubmed_authors>Fauria K</pubmed_authors><pubmed_authors>Hernandez L</pubmed_authors><pubmed_authors>Alvarez PM</pubmed_authors><pubmed_authors>Serra PG</pubmed_authors><pubmed_authors>Escalante AG</pubmed_authors><pubmed_authors>Ballester AP</pubmed_authors><pubmed_authors>Serrat AB</pubmed_authors><pubmed_authors>Molinuevo JL</pubmed_authors><pubmed_authors>Pascual M</pubmed_authors><pubmed_authors>Cacciaglia R</pubmed_authors><pubmed_authors>Penas LH</pubmed_authors><pubmed_authors>Shekari M</pubmed_authors><pubmed_authors>Iglesias RD</pubmed_authors><pubmed_authors>Aguilar RA</pubmed_authors><pubmed_authors>Pradas S</pubmed_authors><pubmed_authors>Ninou JH</pubmed_authors><pubmed_authors>Emilio M</pubmed_authors><pubmed_authors>Martinez AC</pubmed_authors><pubmed_authors>Quevenco FC</pubmed_authors><pubmed_authors>Gorriti AB</pubmed_authors><pubmed_authors>Palacios E</pubmed_authors><pubmed_authors>Cumplido I</pubmed_authors><pubmed_authors>Blennow K</pubmed_authors><pubmed_authors>Jaramillo MV</pubmed_authors><pubmed_authors>Mendez SP</pubmed_authors><pubmed_authors>Mahnaz MS</pubmed_authors><pubmed_authors>Fuentes S</pubmed_authors><pubmed_authors>Sanchez-Benavides G</pubmed_authors><pubmed_authors>Sanchez Benavides GA</pubmed_authors><pubmed_authors>Milan MD</pubmed_authors><pubmed_authors>Karine MEF</pubmed_authors><pubmed_authors>Gispert LC</pubmed_authors><pubmed_authors>ALFA Study</pubmed_authors><pubmed_authors>Freixedes LR</pubmed_authors><pubmed_authors>Rivera OG</pubmed_authors><pubmed_authors>Polo A</pubmed_authors><pubmed_authors>Calvet MS</pubmed_authors><pubmed_authors>Minguillon C</pubmed_authors><pubmed_authors>Diaz TM</pubmed_authors><pubmed_authors>Menchon T</pubmed_authors><pubmed_authors>Prat AS</pubmed_authors><pubmed_authors>Marne P</pubmed_authors><pubmed_authors>Salvado G</pubmed_authors><pubmed_authors>Vilanova M</pubmed_authors><pubmed_authors>Deulofeu C</pubmed_authors><pubmed_authors>Huesa G</pubmed_authors><pubmed_authors>Mila-Aloma M</pubmed_authors><pubmed_authors>Knezevic I</pubmed_authors><pubmed_authors>Gomez CD</pubmed_authors><pubmed_authors>Vila AS</pubmed_authors><pubmed_authors>Fernandez BR</pubmed_authors><pubmed_authors>Tejedor NV</pubmed_authors><pubmed_authors>Julian SF</pubmed_authors><pubmed_authors>Beteta A</pubmed_authors><pubmed_authors>Dominguez R</pubmed_authors><pubmed_authors>Harster LS</pubmed_authors></additional><is_claimable>false</is_claimable><name>The CSF p-tau/β-amyloid 42 ratio correlates with brain structure and fibrillary β-amyloid deposition in cognitively unimpaired individuals at the earliest stages of pre-clinical Alzheimer's disease.</name><description>CSF concentrations of β-amyloid 42 (Aβ42) and phosphorylated tau (p-tau) are well-established biomarkers of Alzheimer's disease and have been studied in relation to several neuropathological features both in patients and in cognitively unimpaired individuals. The CSF p-tau/Aβ42 ratio, a biomarker combining information from both pathophysiological processes, has emerged as a promising tool for monitoring disease progression, even at pre-clinical stages. Here, we studied the association between the CSF p-tau/Aβ42 ratio with downstream markers of pre-clinical Alzheimer's disease progression including brain structure, glucose metabolism, fibrillary Aβ deposition and cognitive performance in 234 cognitively unimpaired individuals, who underwent cognitive testing, a lumbar puncture, MRI, 18F-flu</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025</publication><modification>2026-06-03T04:57:11.285Z</modification><creation>2025-04-05T09:28:30.343Z</creation></dates><accession>S-EPMC11668178</accession><cross_references><pubmed>39723106</pubmed><doi>10.1093/braincomms/fcae451</doi></cross_references></HashMap>