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Alzheimer's disease (AD)

Solute carrier family 25
member 38 (SLC25A38); b-amyloid 42

Human and rodent studies suggest inhibiting SLC25A38 could prevent neurodegeneration in AD. In the brains of patients with AD, SLC25A38 levels were higher than those in healthy controls. In primary rat and mouse neurons and in a human neuroblastoma cell line, b-amyloid 42 increased SLC25A38 levels and caspase-induced apoptosis compared with no treatment. In the rodent primary neurons and the cell line, small interfering RNA against SLC25A38 decreased b-amyloid 42-induced apoptosis compared with control siRNA. Ongoing work includes evaluating the effects of knocking out Slc25a38 in animal AD models.

SciBX 5(44); doi:10.1038/scibx.2012.1164
Published online Nov. 8, 2012

Unpatented; available for licensing or partnering

Zhang, H. et al. J. Neurosci.;
published online Oct. 31, 2012;
Contact: Huaxi Xu, Sanford-Burnham Medical Research Institute, La Jolla, Calif.
Contact: Ye-Guang Chen,
Tsinghua University, Beijing, China