Research ArticleNeurodegeneration
Gain-of-function mutations in protein kinase Cα (PKCα) may promote synaptic defects in Alzheimer’s disease
- Stephanie I. Alfonso1,*,
- Julia A. Callender2,3,*,
- Basavaraj Hooli4,*,
- Corina E. Antal2,3,†,
- Kristina Mullin4,
- Mathew A. Sherman5,
- Sylvain E. Lesné5,
- Michael Leitges6,
- Alexandra C. Newton2,‡,
- Rudolph E. Tanzi4,‡, and
- Roberto Malinow1,‡
- 1Department of Neurosciences and Division of Biology, Section of Neurobiology, University of California, San Diego, La Jolla, CA 92093, USA.
- 2Department of Pharmacology, University of California, San Diego, La Jolla, CA 92093, USA.
- 3Biomedical Sciences Graduate Program, University of California, San Diego, La Jolla, CA 92093, USA.
- 4Genetics and Aging Research Unit, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.
- 5Department of Neuroscience, N. Bud Grossman Center for Memory Research and Care, and Institute for Translational Neuroscience, University of Minnesota, Minneapolis, MN 55414, USA.
- 6Biotechnology Centre of Oslo, University of Oslo, Oslo 0317, Norway.
- ↵‡Corresponding author. Email: anewton{at}ucsd.edu (A.C.N.); tanzi{at}helix.mgh.harvard.edu (R.E.T.); rmalinow{at}ucsd.edu (R.M.)
↵* These authors contributed equally to this work.
↵† Present address: Gene Expression Laboratory, Salk Institute, La Jolla, CA 92037, USA.
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Science Signaling 10 May 2016:
Vol. 9, Issue 427, pp. ra47
DOI: 10.1126/scisignal.aaf6209
