CaV2.1 mediates presynaptic dysfunction induced by amyloid β oligomers

Cell Reports, vol. 44, pp. 115451

Abstract

2.1 haploinsufficiency is sufficient to restore normal neurotransmitter release. These findings reveal a previously unrecognized mechanism driving synaptic dysfunction in AD and identify multiple potentially tractable therapeutic targets.

Authors 8

1. Alexander F. Jeans

   University of Oxford

   Affiliation as printed

   Department of Pharmacology, University of Oxford, Mansfield Road, Oxford OX1 3QT, UK. Electronic address: alexander.jeans@pharm.ox.ac.uk

2. Zahid Padamsey

   University of Oxford

   Affiliation as printed

   Department of Pharmacology, University of Oxford, Mansfield Road, Oxford OX1 3QT, UK

3. Helen Collins

   University of Oxford

   Affiliation as printed

   Department of Pharmacology, University of Oxford, Mansfield Road, Oxford OX1 3QT, UK

4. Sally Allison

   University of Oxford

   Affiliation as printed

   Department of Pharmacology, University of Oxford, Mansfield Road, Oxford OX1 3QT, UK

5. Steven E. Dierksmeier

   University of Oxford

   Affiliation as printed

   Department of Pharmacology, University of Oxford, Mansfield Road, Oxford OX1 3QT, UK

6. William L. Klein

   Northwestern University

   Affiliation as printed

   Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208, USA

7. Arn M. J. M. van den Maagdenberg Aachen Departments of Human Genetics and Neurology

   Leiden University · Leiden University Medical Center

   Affiliation as printed

   Departments of Human Genetics and Neurology, Leiden University Medical Centre, 2300 RC Leiden, the Netherlands

8. Nigel John Emptage

   University of Oxford

   Affiliation as printed

   Department of Pharmacology, University of Oxford, Mansfield Road, Oxford OX1 3QT, UK. Electronic address: nigel.emptage@pharm.ox.ac.uk