Therapeutic correction of ApoER2 splicing in Alzheimer's disease mice using antisense oligonucleotides

Abstract Apolipoprotein E receptor 2 (ApoER2) is an apolipoprotein E receptor involved in long‐term potentiation, learning, and memory. Given its role in cognition and its association with the Alzheimer's disease (AD) risk gene, apoE, ApoER2 has been proposed to be involved in AD, though a role...

Full description

Saved in:
Bibliographic Details
Main Authors: Anthony J Hinrich, Francine M Jodelka, Jennifer L Chang, Daniella Brutman, Angela M Bruno, Clark A Briggs, Bryan D James, Grace E Stutzmann, David A Bennett, Steven A Miller, Frank Rigo, Robert A Marr, Michelle L Hastings
Format: Article
Language:English
Published: Springer Nature 2016-02-01
Series:EMBO Molecular Medicine
Subjects:
Online Access:https://doi.org/10.15252/emmm.201505846
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849331715381657600
author Anthony J Hinrich
Francine M Jodelka
Jennifer L Chang
Daniella Brutman
Angela M Bruno
Clark A Briggs
Bryan D James
Grace E Stutzmann
David A Bennett
Steven A Miller
Frank Rigo
Robert A Marr
Michelle L Hastings
author_facet Anthony J Hinrich
Francine M Jodelka
Jennifer L Chang
Daniella Brutman
Angela M Bruno
Clark A Briggs
Bryan D James
Grace E Stutzmann
David A Bennett
Steven A Miller
Frank Rigo
Robert A Marr
Michelle L Hastings
author_sort Anthony J Hinrich
collection DOAJ
description Abstract Apolipoprotein E receptor 2 (ApoER2) is an apolipoprotein E receptor involved in long‐term potentiation, learning, and memory. Given its role in cognition and its association with the Alzheimer's disease (AD) risk gene, apoE, ApoER2 has been proposed to be involved in AD, though a role for the receptor in the disease is not clear. ApoER2 signaling requires amino acids encoded by alternatively spliced exon 19. Here, we report that the balance of ApoER2 exon 19 splicing is deregulated in postmortem brain tissue from AD patients and in a transgenic mouse model of AD. To test the role of deregulated ApoER2 splicing in AD, we designed an antisense oligonucleotide (ASO) that increases exon 19 splicing. Treatment of AD mice with a single dose of ASO corrected ApoER2 splicing for up to 6 months and improved synaptic function and learning and memory. These results reveal an association between ApoER2 isoform expression and AD, and provide preclinical evidence for the utility of ASOs as a therapeutic approach to mitigate Alzheimer's disease symptoms by improving ApoER2 exon 19 splicing.
format Article
id doaj-art-53d79b4ef2ba4429a49c1630f225c643
institution Kabale University
issn 1757-4676
1757-4684
language English
publishDate 2016-02-01
publisher Springer Nature
record_format Article
series EMBO Molecular Medicine
spelling doaj-art-53d79b4ef2ba4429a49c1630f225c6432025-08-20T03:46:25ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842016-02-018432834510.15252/emmm.201505846Therapeutic correction of ApoER2 splicing in Alzheimer's disease mice using antisense oligonucleotidesAnthony J Hinrich0Francine M Jodelka1Jennifer L Chang2Daniella Brutman3Angela M Bruno4Clark A Briggs5Bryan D James6Grace E Stutzmann7David A Bennett8Steven A Miller9Frank Rigo10Robert A Marr11Michelle L Hastings12Department of Cell Biology and Anatomy, Chicago Medical School, Rosalind Franklin University of Medicine and ScienceDepartment of Cell Biology and Anatomy, Chicago Medical School, Rosalind Franklin University of Medicine and ScienceDepartment of Cell Biology and Anatomy, Chicago Medical School, Rosalind Franklin University of Medicine and ScienceDepartment of Biology, Lake Forest CollegeDepartment of Neuroscience, Chicago Medical School, Rosalind Franklin University of Medicine and ScienceDepartment of Neuroscience, Chicago Medical School, Rosalind Franklin University of Medicine and ScienceRush Alzheimer's Disease Center, Rush University Medical CenterDepartment of Neuroscience, Chicago Medical School, Rosalind Franklin University of Medicine and ScienceRush Alzheimer's Disease Center, Rush University Medical CenterDepartment of Psychology, College of Health Professions, Rosalind Franklin University of Medicine and ScienceIonis PharmaceuticalsDepartment of Neuroscience, Chicago Medical School, Rosalind Franklin University of Medicine and ScienceDepartment of Cell Biology and Anatomy, Chicago Medical School, Rosalind Franklin University of Medicine and ScienceAbstract Apolipoprotein E receptor 2 (ApoER2) is an apolipoprotein E receptor involved in long‐term potentiation, learning, and memory. Given its role in cognition and its association with the Alzheimer's disease (AD) risk gene, apoE, ApoER2 has been proposed to be involved in AD, though a role for the receptor in the disease is not clear. ApoER2 signaling requires amino acids encoded by alternatively spliced exon 19. Here, we report that the balance of ApoER2 exon 19 splicing is deregulated in postmortem brain tissue from AD patients and in a transgenic mouse model of AD. To test the role of deregulated ApoER2 splicing in AD, we designed an antisense oligonucleotide (ASO) that increases exon 19 splicing. Treatment of AD mice with a single dose of ASO corrected ApoER2 splicing for up to 6 months and improved synaptic function and learning and memory. These results reveal an association between ApoER2 isoform expression and AD, and provide preclinical evidence for the utility of ASOs as a therapeutic approach to mitigate Alzheimer's disease symptoms by improving ApoER2 exon 19 splicing.https://doi.org/10.15252/emmm.201505846Alzheimer's diseaseAntisense oligonucleotidesApoER2SplicingTherapeutics
spellingShingle Anthony J Hinrich
Francine M Jodelka
Jennifer L Chang
Daniella Brutman
Angela M Bruno
Clark A Briggs
Bryan D James
Grace E Stutzmann
David A Bennett
Steven A Miller
Frank Rigo
Robert A Marr
Michelle L Hastings
Therapeutic correction of ApoER2 splicing in Alzheimer's disease mice using antisense oligonucleotides
EMBO Molecular Medicine
Alzheimer's disease
Antisense oligonucleotides
ApoER2
Splicing
Therapeutics
title Therapeutic correction of ApoER2 splicing in Alzheimer's disease mice using antisense oligonucleotides
title_full Therapeutic correction of ApoER2 splicing in Alzheimer's disease mice using antisense oligonucleotides
title_fullStr Therapeutic correction of ApoER2 splicing in Alzheimer's disease mice using antisense oligonucleotides
title_full_unstemmed Therapeutic correction of ApoER2 splicing in Alzheimer's disease mice using antisense oligonucleotides
title_short Therapeutic correction of ApoER2 splicing in Alzheimer's disease mice using antisense oligonucleotides
title_sort therapeutic correction of apoer2 splicing in alzheimer s disease mice using antisense oligonucleotides
topic Alzheimer's disease
Antisense oligonucleotides
ApoER2
Splicing
Therapeutics
url https://doi.org/10.15252/emmm.201505846
work_keys_str_mv AT anthonyjhinrich therapeuticcorrectionofapoer2splicinginalzheimersdiseasemiceusingantisenseoligonucleotides
AT francinemjodelka therapeuticcorrectionofapoer2splicinginalzheimersdiseasemiceusingantisenseoligonucleotides
AT jenniferlchang therapeuticcorrectionofapoer2splicinginalzheimersdiseasemiceusingantisenseoligonucleotides
AT daniellabrutman therapeuticcorrectionofapoer2splicinginalzheimersdiseasemiceusingantisenseoligonucleotides
AT angelambruno therapeuticcorrectionofapoer2splicinginalzheimersdiseasemiceusingantisenseoligonucleotides
AT clarkabriggs therapeuticcorrectionofapoer2splicinginalzheimersdiseasemiceusingantisenseoligonucleotides
AT bryandjames therapeuticcorrectionofapoer2splicinginalzheimersdiseasemiceusingantisenseoligonucleotides
AT graceestutzmann therapeuticcorrectionofapoer2splicinginalzheimersdiseasemiceusingantisenseoligonucleotides
AT davidabennett therapeuticcorrectionofapoer2splicinginalzheimersdiseasemiceusingantisenseoligonucleotides
AT stevenamiller therapeuticcorrectionofapoer2splicinginalzheimersdiseasemiceusingantisenseoligonucleotides
AT frankrigo therapeuticcorrectionofapoer2splicinginalzheimersdiseasemiceusingantisenseoligonucleotides
AT robertamarr therapeuticcorrectionofapoer2splicinginalzheimersdiseasemiceusingantisenseoligonucleotides
AT michellelhastings therapeuticcorrectionofapoer2splicinginalzheimersdiseasemiceusingantisenseoligonucleotides