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...

Descripción completa

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
_version_ 1782425073521524736
author Wasser, Catherine R
Herz, Joachim
author_facet Wasser, Catherine R
Herz, Joachim
author_sort Wasser, Catherine R
collection PubMed
description 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.
format Online
Article
Text
id pubmed-4818748
institution National Center for Biotechnology Information
language English
publishDate 2016
publisher John Wiley and Sons Inc.
record_format MEDLINE/PubMed
spelling pubmed-48187482016-04-14 Splicing therapeutics for Alzheimer's disease Wasser, Catherine R Herz, Joachim EMBO Mol Med News & Views 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. John Wiley and Sons Inc. 2016-02-22 2016-04 /pmc/articles/PMC4818748/ /pubmed/26902203 http://dx.doi.org/10.15252/emmm.201506067 Text en © 2016 The Authors. Published under the terms of the CC BY 4.0 license This is an open access article under the terms of the Creative Commons Attribution 4.0 (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle News & Views
Wasser, Catherine R
Herz, Joachim
Splicing therapeutics for Alzheimer's disease
title Splicing therapeutics for Alzheimer's disease
title_full Splicing therapeutics for Alzheimer's disease
title_fullStr Splicing therapeutics for Alzheimer's disease
title_full_unstemmed Splicing therapeutics for Alzheimer's disease
title_short Splicing therapeutics for Alzheimer's disease
title_sort splicing therapeutics for alzheimer's disease
topic News & Views
url 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
work_keys_str_mv AT wassercatheriner splicingtherapeuticsforalzheimersdisease
AT herzjoachim splicingtherapeuticsforalzheimersdisease

Ejemplares similares