Splicing therapeutics for Alzheimer'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 (Apoer...

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Detalles Bibliográficos
Autores principales: Wasser, Catherine R, Herz, Joachim
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2016
Materias:
News & Views
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4818748/
https://www.ncbi.nlm.nih.gov/pubmed/26902203
http://dx.doi.org/10.15252/emmm.201506067
Descripción
Sumario: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.

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