Supplementary Materials

Supplementary Materials for:

Gain-of-function mutations in protein kinase Cα (PKCα) may promote synaptic defects in Alzheimer's disease

Stephanie I. Alfonso, Julia A. Callender, Basavaraj Hooli, Corina E. Antal, Kristina Mullin, Mathew A. Sherman, Sylvain E. Lesné, Michael Leitges, Alexandra C. Newton,* Rudolph E. Tanzi,* Roberto Malinow*

*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.)

This PDF file includes:

  • Fig. S1. Aβ abundance in brain slices infected with virus producing CT100 is similar in wild-type and PRKCA−/− slices.
  • Fig. S2. Pedigree charts of the NIMH families found to carry rare PKCα variants.

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Citation: S. I. Alfonso, J. A. Callender, B. Hooli, C. E. Antal, K. Mullin, M. A. Sherman, S. E. Lesné, M. Leitges, A. C. Newton, R. E. Tanzi, R. Malinow, Gain-of-function mutations in protein kinase Cα (PKCα) may promote synaptic defects in Alzheimer's disease. Sci. Signal. 9, ra47 (2016).

© 2016 American Association for the Advancement of Science