Gain-of-function mutations in protein kinase Cα (PKCα) may promote synaptic defects in Alzheimer’s disease-Reference-Cited by-同舟云学术

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

Published:2016-05-10 Issue:427 Volume:9 Page:
ISSN:1945-0877
Container-title:Science Signaling
language:en
Short-container-title:Sci. Signal.

Author:

Alfonso Stephanie I.¹,Callender Julia A.²³,Hooli Basavaraj⁴,Antal Corina E.²³,Mullin Kristina⁴,Sherman Mathew A.⁵,Lesné Sylvain E.⁵,Leitges Michael⁶,Newton Alexandra C.²,Tanzi Rudolph E.⁴,Malinow Roberto¹

Affiliation:

1. Department of Neurosciences and Division of Biology, Section of Neurobiology, University of California, San Diego, La Jolla, CA 92093, USA.

2. Department of Pharmacology, University of California, San Diego, La Jolla, CA 92093, USA.

3. Biomedical Sciences Graduate Program, University of California, San Diego, La Jolla, CA 92093, USA.

4. Genetics and Aging Research Unit, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.

5. Department of Neuroscience, N. Bud Grossman Center for Memory Research and Care, and Institute for Translational Neuroscience, University of Minnesota, Minneapolis, MN 55414, USA.

6. Biotechnology Centre of Oslo, University of Oslo, Oslo 0317, Norway.

Abstract

PKCα variants in some patients with Alzheimer’s disease may mediate the pathological effects of amyloid-β.

Funder

NIH

Cure Alzheimer's Fund

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Cell Biology,Molecular Biology,Biochemistry

Reference53 articles.

1. Physical basis of cognitive alterations in alzheimer's disease: Synapse loss is the major correlate of cognitive impairment