PP2A methylation controls sensitivity and resistance to β-amyloid–induced cognitive and electrophysiological impairments
Abstract
Elevated levels of the β-amyloid peptide (Aβ) are thought to contribute to the cognitive impairments associated with Alzheimer’s disease (AD). We found that by genetically targeting the methylation of protein phosphatase 2A (PP2A) in transgenic mice, we could alter the sensitivity of animals to electrophysiological and cognitive impairments caused by Aβ exposure without affecting Aβ production or the electrophysiological response to low concentrations of Aβ. These data support a role for PP2A methylation in contributing to AD risk and identify a potential therapeutic pathway that might be exploited to target the pathological actions of Aβ selectively.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Mar 07, 2016
- Source ID
- 10.1073/pnas.1521018113
Entities
People
- Agnieszka Staniszewski
- Brandi Wasek
- Caitlin M. Woodruff
- Carla Y. Kim
- Deqi Yin
- Eric R. Kandel
- Erland Arning
- Estelle Sontag
- Hong Zhang
- Jean-marie Sontag
- Michael Yim
- Ottavio Arancio
- Russell E. Nicholls
- Shijun Yan
- Teodoro Bottiglieri
Organizations
- Baylor University
- Columbia University
- Congressionally Directed Medical Research Programs
- Hunter Medical Research Institute
- National Health and Medical Research Council
- National Institute of Neurological Disorders and Stroke
- University of Newcastle