期刊论文

Li, L

英文

Neuroscience

0306-4522

2018

373

1

207-217

10.1016/j.neuroscience.2018.01.026

We thank Dr. Martin Bergo for providing the original breeding pairs for GGT-haplodeficient and GGT floxed mice and Emily Leathley for assistance with electrophysiology experiments. We also thank Drs. Gibson Wood and Mark Distefano for helpful discussions on the data. This work was supported in part by grants from the National Institute on Aging of the National Institutes of Health (AG056976 and AG056025), and the College of Pharmacy and the Academic Health Center of the University of Minnesota to LL. DH was supported by an NIH pre-doctoral training fellowship (AG029796) and the Bighley/Rowell Graduate fellowship from the College of Pharmacy at the University of Minnesota. We thank Dr. Martin Bergo for providing the original breeding pairs for GGT-haplodeficient and GGT floxed mice and Emily Leathley for assistance with electrophysiology experiments. We also thank Drs. Gibson Wood and Mark Distefano for helpful discussions on the data. This work was supported in part by grants from the National Institute on Aging of the National Institutes of Health ( AG056976 and AG056025 ), and the College of Pharmacy and the Academic Health Center of the University of Minnesota to LL. DH was supported by an NIH pre-doctoral training fellowship ( AG029796 ) and the Bighley/Rowell Graduate fellowship from the College of Pharmacy at the University of Minnesota .

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Isoprenoids and prenylated proteins regulate a variety of cellular functions, including neurite growth and synaptic plasticity. Importantly, they are implicated in the pathogenesis of several diseases, including Alzheimer's disease (AD). Recently, we have shown that two protein prenyltransferases, farnesyltransferase (FT) and geranylgeranyltransferase-1 (GGT), have differential effects in a mouse model of AD. Haplodeficiency of either FT or GGT attenuates amyloid-β deposition and neuroinflammation but only reduction in FT rescues cognitive fun...