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

https://doi.org/10.15252/emmm.201505846

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What this work says

Outgoing claims: the papers this work cites, builds on, or argues with.

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Targeting RNA splicing for disease therapy

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Apolipoprotein E in sporadic Alzheimer's disease: Allelic variation and receptor interactions

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Antisense Masking of an hnRNP A1/A2 Intronic Splicing Silencer Corrects SMN2 Splicing in Transgenic Mice

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Selenoprotein P—Expression, functions, and roles in mammals

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Spatial learning and memory impairment and increased locomotion in a transgenic amyloid precursor protein mouse model of Alzheimer's disease

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Integrative Genome-wide Analysis Reveals Cooperative Regulation of Alternative Splicing by hnRNP Proteins

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ApoE Receptor 2 Controls Neuronal Survival in the Adult Brain

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Carvedilol as a potential novel agent for the treatment of Alzheimer's disease

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Modulation of Synaptic Plasticity and Memory by Reelin Involves Differential Splicing of the Lipoprotein Receptor Apoer2

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ApoE and Aβ in Alzheimer’s Disease: Accidental Encounters or Partners?

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LRP8-Reelin-Regulated Neuronal Enhancer Signature Underlying Learning and Memory Formation

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Decisive role of Reelin signaling during early stages of Alzheimer’s disease

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Expression and alternate splicing of apolipoprotein E receptor 2 in brain

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APP Processing and Synaptic Function

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Impaired synaptic plasticity and learning in aged amyloid precursor protein transgenic mice

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c-Jun N-terminal kinase has a key role in Alzheimer disease synaptic dysfunction in vivo

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Reelin delays amyloid-beta fibril formation and rescues cognitive deficits in a model of Alzheimer’s disease

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Rescue of hearing and vestibular function by antisense oligonucleotides in a mouse model of human deafness

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Cleavage of tau by asparagine endopeptidase mediates the neurofibrillary pathology in Alzheimer's disease

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Regulation of NMDA receptor trafficking by amyloid-β

inferredcites →https://doi.org/10.1038/nprot.2006.116openalex-snapshot

Morris water maze: procedures for assessing spatial and related forms of learning and memory

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RNA therapeutics: beyond RNA interference and antisense oligonucleotides

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Reelin, lipoprotein receptors and synaptic plasticity

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A balance between excitatory and inhibitory synapses is controlled by PSD-95 and neuroligin

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Early-onset behavioral and synaptic deficits in a mouse model of Alzheimer's disease

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Reelin signaling antagonizes β-amyloid at the synapse

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U1 small nuclear ribonucleoprotein complex and RNA splicing alterations in Alzheimer’s disease

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2′-O-(2-Methoxy)ethyl-modified Anti-intercellular Adhesion Molecule 1 (ICAM-1) Oligonucleotides Selectively Increase the ICAM-1 mRNA Level and Inhibit Formation of the ICAM-1 Translation Initiation Complex in Human Umbilical Vein Endothelial Cells

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Interaction of Cytosolic Adaptor Proteins with Neuronal Apolipoprotein E Receptors and the Amyloid Precursor Protein

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Interactions of the Low Density Lipoprotein Receptor Gene Family with Cytosolic Adaptor and Scaffold Proteins Suggest Diverse Biological Functions in Cellular Communication and Signal Transduction

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Reelin and ApoE Receptors Cooperate to Enhance Hippocampal Synaptic Plasticity and Learning

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Targeting SR Proteins Improves SMN Expression in Spinal Muscular Atrophy Cells

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Reduced Reelin Expression Accelerates Amyloid- Plaque Formation and Tau Pathology in Transgenic Alzheimer's Disease Mice

inferredcites →https://doi.org/10.1523/jneurosci.21-13-04691.2001openalex-snapshot

Age-Related Impairment of Synaptic Transmission But Normal Long-Term Potentiation in Transgenic Mice that Overexpress the Human APP695SWE Mutant Form of Amyloid Precursor Protein

inferredcites →https://doi.org/10.1523/jneurosci.3028-12.2012openalex-snapshot

Beta Amyloid-Induced Depression of Hippocampal Long-Term Potentiation Is Mediated through the Amylin Receptor

inferredcites →https://doi.org/10.1523/jneurosci.3758-06.2007openalex-snapshot

Reelin Depletion in the Entorhinal Cortex of Human Amyloid Precursor Protein Transgenic Mice and Humans with Alzheimer's Disease

inferredcites →https://doi.org/10.1523/jneurosci.3993-06.2007openalex-snapshot

Apolipoprotein Receptor 2 and X11α/β Mediate Apolipoprotein E-Induced Endocytosis of Amyloid-β Precursor Protein and β-Secretase, Leading to Amyloid-β Production

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Reelin Depletion is an Early Phenomenon of Alzheimer's Pathology

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Gene Expression Changes Related to Synaptic Deficits in the Tg2576 Mouse Model of Alzheimer’s Disease

What points at this work

Incoming claims: where this work appears in other papers’ reference lists and arguments.

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Antisense oligonucleotide therapy corrects splicing in the common Stargardt disease type 1-causing variant ABCA4 c.5461-10T>C

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inferred← citeshttps://doi.org/10.1194/jlr.r075507openalex-snapshot

The ApoE receptors Vldlr and Apoer2 in central nervous system function and disease

inferred← citeshttps://doi.org/10.1212/nxg.0000000000000323openalex-snapshot

Antisense oligonucleotides

inferred← citeshttps://doi.org/10.12997/jla.2022.11.2.133openalex-snapshot

Exploring the Genetic Associations Between the Use of Statins and Alzheimer's Disease

inferred← citeshttps://doi.org/10.1371/journal.pgen.1011348openalex-snapshot

APOER2 splicing repertoire in Alzheimer’s disease: Insights from long-read RNA sequencing

inferred← citeshttps://doi.org/10.1523/jneurosci.1054-16.2016openalex-snapshot

Genetic Restoration of Plasma ApoE Improves Cognition and Partially Restores Synaptic Defects in ApoE-Deficient Mice

inferred← citeshttps://doi.org/10.1523/jneurosci.1388-25.2025openalex-snapshot

APOE-Targeted Therapeutics for Alzheimer's Disease

inferred← citeshttps://doi.org/10.15252/emmm.201506067openalex-snapshot

Splicing therapeutics for Alzheimer's disease

inferred← citeshttps://doi.org/10.1590/1678-4324-2017160481openalex-snapshot

A Mechanism Study of NMDAR1 in A Rat Alzheimer Disease (AD) Model

inferred← citeshttps://doi.org/10.21203/rs.3.rs-2200020/v1openalex-snapshot

A TDP-43 acetylation-mimic mutation that disrupts RNA-binding drives FTLD-like neurodegeneration in a mouse model of sporadic TDP-43 proteinopathy

inferred← citeshttps://doi.org/10.21203/rs.3.rs-2200020/v2openalex-snapshot

RNA-binding deficient TDP-43 drives cognitive decline in a mouse model of TDP-43 proteinopathy

inferred← citeshttps://doi.org/10.21203/rs.3.rs-2200020/v3openalex-snapshot

RNA-binding deficient TDP-43 drives cognitive decline in a mouse model of TDP-43 proteinopathy

inferred← citeshttps://doi.org/10.21203/rs.3.rs-2200020/v4openalex-snapshot

RNA-binding deficient TDP-43 drives cognitive decline in a mouse model of TDP-43 proteinopathy

inferred← citeshttps://doi.org/10.21203/rs.3.rs-2200020/v5openalex-snapshot

RNA-binding deficient TDP-43 drives cognitive decline in a mouse model of TDP-43 proteinopathy

inferred← citeshttps://doi.org/10.2139/ssrn.7435655openalex-snapshot

ALS-Associated Exitron Splicing Produces UBQLN2 Isoforms with Distinct Properties

inferred← citeshttps://doi.org/10.2174/1386207325666220428112541openalex-snapshot

NMDA Inhibitors: A Potential Contrivance to Assist in Management of Alzheimer’s Disease

inferred← citeshttps://doi.org/10.2174/1389557520666200513122357openalex-snapshot

A Systematic Review of Current Progresses in the Nucleic Acid-Based Therapies for Neurodegeneration with Implications for Alzheimer’s Disease

inferred← citeshttps://doi.org/10.31491/apt.2022.12.100openalex-snapshot

Evidence for an alternative insulin transporter at the blood-brain barrier

inferred← citeshttps://doi.org/10.3233/jad-179939openalex-snapshot

Religious Orders Study and Rush Memory and Aging Project

inferred← citeshttps://doi.org/10.3233/jad-190914openalex-snapshot

Carnosic Acid Reverses the Inhibition of ApoE4 on Cell Surface Level of ApoER2 and Reelin Signaling Pathway

inferred← citeshttps://doi.org/10.3233/jad-220071openalex-snapshot

Lipid Peroxidation Induced ApoE Receptor-Ligand Disruption as a Unifying Hypothesis Underlying Sporadic Alzheimer’s Disease in Humans

inferred← citeshttps://doi.org/10.3233/jad-220758openalex-snapshot

Lithium Provides Broad Therapeutic Benefits in an Alzheimer’s Disease Mouse Model

inferred← citeshttps://doi.org/10.3389/fcell.2022.994588openalex-snapshot

Tsukushi proteoglycan maintains RNA splicing and developmental signaling network in GFAP-expressing subventricular zone neural stem/progenitor cells

inferred← citeshttps://doi.org/10.3389/fgene.2022.926049openalex-snapshot

Ontology Specific Alternative Splicing Changes in Alzheimer’s Disease

inferred← citeshttps://doi.org/10.3389/fmolb.2018.00012openalex-snapshot

Alternative Splicing in Neurogenesis and Brain Development

inferred← citeshttps://doi.org/10.3389/fnagi.2021.755392openalex-snapshot

Brain Pathogenesis and Potential Therapeutic Strategies in Myotonic Dystrophy Type 1

inferred← citeshttps://doi.org/10.3389/fnagi.2023.1199434openalex-snapshot

Neuronal ApoE4 in Alzheimer’s disease and potential therapeutic targets

inferred← citeshttps://doi.org/10.3389/fnins.2019.01103openalex-snapshot

MicroRNAs Dysregulation and Metabolism in Multiple System Atrophy

inferred← citeshttps://doi.org/10.3389/fnins.2021.630502openalex-snapshot

APOE and Alzheimer’s Disease: From Lipid Transport to Physiopathology and Therapeutics

inferred← citeshttps://doi.org/10.3389/fnmol.2017.00054openalex-snapshot

Functional Roles of the Interaction of APP and Lipoprotein Receptors

inferred← citeshttps://doi.org/10.3389/fnmol.2020.00144openalex-snapshot

ApoER2: Functional Tuning Through Splicing

inferred← citeshttps://doi.org/10.3389/fnmol.2024.1391564openalex-snapshot

Down syndrome and DYRK1A overexpression: relationships and future therapeutic directions

inferred← citeshttps://doi.org/10.3389/fphar.2022.1006304openalex-snapshot

A perspective on oligonucleotide therapy: Approaches to patient customization

inferred← citeshttps://doi.org/10.3390/cells11050840openalex-snapshot

What’s in a Gene? The Outstanding Diversity of MAPT

inferred← citeshttps://doi.org/10.3390/ijms19103090openalex-snapshot

The Reelin Receptors Apolipoprotein E receptor 2 (ApoER2) and VLDL Receptor

inferred← citeshttps://doi.org/10.3390/ijms23010462openalex-snapshot

Relevance of a Novel Circuit-Level Model of Episodic Memories to Alzheimer’s Disease

inferred← citeshttps://doi.org/10.3390/ijms23168921openalex-snapshot

Low-Density Lipoprotein Receptor-Related Protein 8 at the Crossroad between Cancer and Neurodegeneration

inferred← citeshttps://doi.org/10.3390/ijms25063391openalex-snapshot

A Precision Therapy Approach for Retinitis Pigmentosa 11 Using Splice-Switching Antisense Oligonucleotides to Restore the Open Reading Frame of PRPF31

inferred← citeshttps://doi.org/10.3390/molecules30173479openalex-snapshot

Biologics as Therapeutical Agents Under Perspective Clinical Studies for Alzheimer’s Disease

inferred← citeshttps://doi.org/10.3390/pharmaceutics14081708openalex-snapshot

Towards Personalized Allele-Specific Antisense Oligonucleotide Therapies for Toxic Gain-of-Function Neurodegenerative Diseases

inferred← citeshttps://doi.org/10.4236/aad.2023.124005openalex-snapshot

Presymptomatic Diagnosis and Gene Therapy for Alzheimer’s Disease: Genomic, Therapeutic, and Ethical Aspects—A Systematic Review

inferred← citeshttps://doi.org/10.5213/inj.2244258.129openalex-snapshot

Brain Region-Dependent Alternative Splicing of Alzheimer Disease (AD)-Risk Genes Is Associated With Neuropathological Features in AD

inferred← citeshttps://doi.org/10.55730/1300-0152.2683openalex-snapshot

Effect of thymol on oxidative stress and reelin signaling pathway in Alzheimer's disease model

inferred← citeshttps://doi.org/10.6084/m9.figshare.22621606openalex-snapshot

Additional file 2 of Differential splicing of neuronal genes in a Trem2*R47H mouse model mimics alterations associated with Alzheimer’s disease

inferred← citeshttps://doi.org/10.64898/2026.07.02.736008openalex-snapshot

HnRNPAB -targeted antisense oligonucleotides ameliorate tau pathology and cognitive deficits by modulating Alzheimer’s disease-associated alternative splicing

inferred← citeshttps://doi.org/10.70675/39639c36z8ae3z4f14z9907zaaead2a13436openalex-snapshot

Modulation of hippo pathway by alternative splicing

inferred← citeshttps://doi.org/10.70675/759ed785ze142z4504za8abzd5cf222c1a59openalex-snapshot

Développement d'anticorps à domaine unique comme vecteurs ciblant des récepteurs impliqués dans la transcytose et traversant la barrière hémato-encéphalique pour l'adressage d'agents d'imagerie et thérapeutiques vers le cerveau

inferred← citeshttps://doi.org/10.7150/thno.21529openalex-snapshot

Nucleic Acid-Based Theranostics for Tackling Alzheimer's Disease

inferred← citeshttps://doi.org/10.7554/elife.85921openalex-snapshot

RNA-binding deficient TDP-43 drives cognitive decline in a mouse model of TDP-43 proteinopathy

inferred← citeshttps://doi.org/10.7554/elife.85921.1openalex-snapshot

RNA-binding deficient TDP-43 drives cognitive decline in a mouse model of TDP-43 proteinopathy

inferred← citeshttps://doi.org/10.7554/elife.85921.1.sa0openalex-snapshot

Reviewer #3 (Public Review): RNA-binding deficient TDP-43 drives cognitive decline in a mouse model of TDP-43 proteinopathy

inferred← citeshttps://doi.org/10.7554/elife.85921.1.sa1openalex-snapshot

Reviewer #2 (Public Review): RNA-binding deficient TDP-43 drives cognitive decline in a mouse model of TDP-43 proteinopathy

inferred← citeshttps://doi.org/10.7554/elife.85921.1.sa2openalex-snapshot

Reviewer #1 (Public Review): RNA-binding deficient TDP-43 drives cognitive decline in a mouse model of TDP-43 proteinopathy

inferred← citeshttps://doi.org/10.7554/elife.85921.1.sa3openalex-snapshot

eLife Assessment: RNA-binding deficient TDP-43 drives cognitive decline in a mouse model of TDP-43 proteinopathy

inferred← citeshttps://doi.org/10.7554/elife.85921.2openalex-snapshot

RNA-binding deficient TDP-43 drives cognitive decline in a mouse model of TDP-43 proteinopathy

inferred← citeshttps://doi.org/10.7554/elife.85921.3openalex-snapshot

RNA-binding deficient TDP-43 drives cognitive decline in a mouse model of TDP-43 proteinopathy

Editorial review for independent work. ICSAC — the Institute for Complexity Science and Advanced Computing — runs a structured editorial panel for researchers publishing outside journals, and publishes on CiteStamp rails. Submission is free and goes through ORCID: icsacinstitute.org/submit.