TY - JOUR
T1 - Splicing therapeutics for Alzheimer's disease
AU - Wasser, Catherine R.
AU - Herz, Joachim
N1 - Publisher Copyright:
© 2016 EMBO.
PY - 2016/4/1
Y1 - 2016/4/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=84958725974&partnerID=8YFLogxK
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U2 - 10.15252/emmm.201506067
DO - 10.15252/emmm.201506067
M3 - Comment/debate
C2 - 26902203
AN - SCOPUS:84958725974
SN - 1757-4676
VL - 8
SP - 308
EP - 310
JO - EMBO Molecular Medicine
JF - EMBO Molecular Medicine
IS - 4
ER -