Splicing therapeutics for Alzheimer's disease

EMBO Mol Med. 2016 Apr 1;8(4):308-10. doi: 10.15252/emmm.201506067.

Abstract

The earliest clinical manifestation of Alzheimer's disease (AD) is cognitive impairment caused by synaptic dysfunction. ApoE4, the primary risk factor for late‐onset AD, disrupts synaptic homeostasis by impairing synaptic ApoE receptor trafficking. Alternative splicing of ApoE receptor‐2 (Apoer2) maintains synaptic homeostasis. In this issue, Hinrich et al (2016) show that Apoer2 splicing is impaired in human AD brains and murine AD models and that restoring normal splicing in the mouse rescues amyloid‐induced cognitive defects.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Comment

MeSH terms

  • Alzheimer Disease*
  • Amyloid beta-Peptides
  • Humans
  • RNA Splicing*

Substances

  • Amyloid beta-Peptides