Negative / Null Result ReportOpen accessMedicine· cited by 84

Treatment with bexarotene, a compound that increases apolipoprotein-E, provides no cognitive benefit in mutant APP/PS1 mice

Katherine D. LaClair; Kebreten F. Manaye; Dexter L. Lee; Joanne Allard; Alena Savonenko; Juan C. Troncoso; Philip C. Wong · 2013 · Molecular Neurodegeneration

WASTE classifies this as Negative / Null Result Report · AI classification, approximate

The study found no significant effect — useful as a negative control or null benchmark for your own design.

Abstract

BACKGROUND: Though the precise cause(s) of Alzheimer's disease (AD) remain unknown, there is strong evidence that decreased clearance of β-amyloid (Aβ) from the brain can contribute to the disease. Therapeutic strategies to promote natural Aβ clearance mechanisms, such as the protein apolipoprotein-E (APOE), hold promise for the treatment of AD. The amount of APOE in the brain is regulated by nuclear receptors including retinoid X receptors (RXRs). Drugs that activate RXRs, including bexarotene, can increase APOE and ABCA1 production, and have been shown to decrease the Aβ burden and improve c

Abstract by Katherine D. LaClair; Kebreten F. Manaye; Dexter L. Lee; Joanne Allard; Alena Savonenko; Juan C. Troncoso; Philip C. Wong, Molecular Neurodegeneration (2013) — licensed CC BY 4.0.

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