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Retinol Binding Protein 4 Levels Are Not Altered in Preclinical Alzheimer's Disease and Not Associated with Cognitive Decline or Incident Dementia.

TitleRetinol Binding Protein 4 Levels Are Not Altered in Preclinical Alzheimer's Disease and Not Associated with Cognitive Decline or Incident Dementia.
Publication TypeJournal Article
Year of Publication2019
AuthorsIshii M, Kamel H, Iadecola C
JournalJ Alzheimers Dis
Volume67
Issue1
Pagination257-263
Date Published2019
ISSN1875-8908
KeywordsAged, Aged, 80 and over, Alzheimer Disease, Amyloid beta-Peptides, Biomarkers, Cognitive Dysfunction, Dementia, Female, Follow-Up Studies, Humans, Incidence, Longitudinal Studies, Male, Negative Results, Peptide Fragments, Retinol-Binding Proteins, Plasma, tau Proteins
Abstract

Accumulating evidence suggests that disparate pathways from systemic metabolism to retinoic acid/vitamin A signaling can contribute to Alzheimer's disease (AD) pathobiology. Retinol binding protein 4 (RBP4) is an adipocyte-secreted hormone (adipokine) that regulates insulin signaling and is also a key transporter of retinoic acid and its derivatives. While earlier studies found alterations in the brain and cerebrospinal fluid (CSF) levels of RBP4 in later stages of AD, it is not known if circulating RBP4 is altered in preclinical AD or if it can be a useful biomarker for cognitive decline and dementia. In this study, we used ELISA to measure plasma RBP4 levels in cognitively normal individuals (Clinical Dementia Rating, CDR 0). Subjects with preclinical AD were identified by previously established CSF criteria (preclinical AD: 20 men, 18 women; control: 45 men, 73 women). Plasma RBP4 levels were similar between preclinical AD and control subjects in men (preclinical AD: 30.0±7.4 μg/mL; control: 30.0±8.7 μg/mL; p = 0.97) and women (preclinical AD 30.9±7.9 μg/mL; control: 31.7±8.5 μg/mL; p = 0.72). Additionally, RBP4 levels were not related to body mass index or CSF AD biomarkers levels of amyloid-β42, tau, or phosphorylated tau. Baseline plasma RBP4 levels were not associated with the incidence of CDR ≥0.5, all-cause dementia, or AD diagnosis. Collectively, these results do not support peripheral RBP4 as a clinical biomarker or therapeutic target in the early stages of AD.

DOI10.3233/JAD-180682
Alternate JournalJ. Alzheimers Dis.
PubMed ID30562901
PubMed Central IDPMC6385158
Grant ListR01 NS037853 / NS / NINDS NIH HHS / United States
P01 AG003991 / AG / NIA NIH HHS / United States
K08 AG051179 / AG / NIA NIH HHS / United States
P50 AG005681 / AG / NIA NIH HHS / United States
K23 NS082367 / NS / NINDS NIH HHS / United States
P01 AG026276 / AG / NIA NIH HHS / United States

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