Affiliations: [a] School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, NSW, Australia | [b] Illawarra Health and Medical Research Institute and The School of Biological Sciences, University of Wollongong, Wollongong, NSW, Australia | [c] Neuroscience Research Australia and University of New South Wales, Sydney, NSW, Australia
Correspondence:
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Correspondence to: Andrew J. Brown, BABS, School of Biotechnology and Biomolecular Sciences, Biological Sciences Building D26, University of New South Wales, Sydney, NSW 2052, Australia. Tel.: +61 2 9385 2005; Fax: +61 2 9385 1483; E-mail: [email protected].
Note: [1] These authors contributed equally to this work.
Abstract: Selective Alzheimer's Disease Indicator-1 (Seladin-1) was originally identified by its down-regulation in the brains of Alzheimer's disease (AD) patients. Here, we re-examine existing data and present new gene expression data that refutes its role as a selective AD indicator. Furthermore, we caution against the use of the name “Seladin-1” and instead recommend adoption of the approved nomenclature, 3β-hydroxysterol Δ24-reductase (or DHCR24), which describes its catalytic function in cholesterol synthesis. Further work is required to determine what link, if any, exists between DHCR24 and AD.
