Splicing therapeutics for Alzheimer's disease

Catherine R. Wasser, Joachim Herz

Research output: Contribution to journalComment/debatepeer-review

3 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)308-310
Number of pages3
JournalEMBO Molecular Medicine
Volume8
Issue number4
DOIs
StatePublished - Apr 1 2016

ASJC Scopus subject areas

  • Molecular Medicine

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