Splicing therapeutics for Alzheimer's disease

Catherine R. Wasser, Joachim Herz

Research output: Contribution to journalArticle

2 Citations (Scopus)

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 () 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)
JournalEMBO Molecular Medicine
DOIs
StateAccepted/In press - 2016

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Low Density Lipoprotein Receptor-Related Protein-1
Alzheimer Disease
Homeostasis
Apolipoprotein E4
Neurotransmitter Receptor
Alternative Splicing
Therapeutics
Amyloid
Brain

ASJC Scopus subject areas

  • Molecular Medicine

Cite this

Splicing therapeutics for Alzheimer's disease. / Wasser, Catherine R.; Herz, Joachim.

In: EMBO Molecular Medicine, 2016.

Research output: Contribution to journalArticle

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