Splicing therapeutics for A lzheimer's disease

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.

Object Details

• Location: Deutsche Nationalbibliothek Frankfurt am Main
• Extent: Online-Ressource
• Language: Englisch

References and Relationships

• Bibliographic citation: Splicing therapeutics for A lzheimer's disease ; volume:8 ; number:4 ; year:2016 ; pages:308-310 ; extent:3 ; EMBO molecular medicine / European Molecular Biology Organization ; 8, Heft 4 (2016), 308-310 (gesamt 3)

Contributors, Places and Time

• Creator: Wasser, Catherine R. ; Herz, Joachim

Further information

• DOI: 10.15252/emmm.201506067
• URN: urn:nbn:de:101:1-2022111305255285288871
• Rights: Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
• Last update: 15.08.2025, 7:20 AM CEST