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Home › Research › Topics › antisense-oligonucleotide

antisense-oligonucleotide

16 studies tagged antisense-oligonucleotide, dated 1994-10-01 to 2025-05-01. Bibliography: BibTeX (.bib) · RIS (.ris)

Newest in this topic

  1. Antisense oligonucleotides directed against App and Rab5 normalized endosomal Rab activity and reversed DS-AD-linked degenerative phenotypes in the Dp16 mouse model of Down syndrome 2025-05-01
  2. A splice-switching antisense oligonucleotide targeting APP reduces accumulation of α-synuclein in a mouse model of Parkinson's disease 2025-04-01
  3. Correcting tau isoform ratios with a long-acting antisense oligonucleotide alleviates 4R-tauopathy phenotypes 2025-03-05

Studies

16 studies carry this tag.

Date range

1994 to 2025

Top journals

  • Journal of Alzheimer's disease : JAD 3
  • Acta neuropathologica 1
  • Alzheimer's & dementia (New York, N. Y.) 1
  • Alzheimer's & dementia : the journal of the Alzheimer's Association 1
  • Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis 1

14 journals in all.

Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.

  1. Antisense oligonucleotides directed against App and Rab5 normalized endosomal Rab activity and reversed DS-AD-linked degenerative phenotypes in the Dp16 mouse model of Down syndrome

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2025-05-01 Drug development

    These findings highlight ELN dysregulation in DS and the therapeutic potential of ASO-based strategies targeting APP or Rab5 to counteract DS-AD features.

  2. A splice-switching antisense oligonucleotide targeting APP reduces accumulation of α-synuclein in a mouse model of Parkinson's disease

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Alzheimer's & dementia (New York, N. Y.) 2025-04-01 Drug development

    Our findings demonstrate that targeting APP reduces α-syn pathology and rescues neuronal loss, supporting the therapeutic potential of APP modulation in synucleinopathies.

  3. Correcting tau isoform ratios with a long-acting antisense oligonucleotide alleviates 4R-tauopathy phenotypes

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Molecular therapy. Nucleic acids 2025-03-05 Drug development

    Tau, a microtubule-binding protein linked to tauopathies like Alzheimer's disease and frontotemporal lobar degeneration (FTLD), has 3-repeat (3R) and 4-repeat (4R) isoforms.

  4. G2C4 targeting antisense oligonucleotides potently mitigate TDP-43 dysfunction in human C9orf72 ALS/FTD induced pluripotent stem cell derived neurons

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Acta neuropathologica 2023-11-29 Drug development

    The G 4 C 2 repeat expansion in the C9orf72 gene is the most common genetic cause of Amyotrophic Lateral Sclerosis and Frontotemporal Dementia.

  5. Novel systemic delivery of a peptide-conjugated antisense oligonucleotide to reduce α-synuclein in a mouse model of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Neurobiology of disease 2023-09-09 Drug development

    Neurodegenerative disorders of aging are characterized by the progressive accumulation of proteins such as α-synuclein (α-syn) and amyloid beta (Aβ).

  6. A physiologically-based pharmacokinetic model to describe antisense oligonucleotide distribution after intrathecal administration

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of pharmacokinetics and pharmacodynamics 2021-05-15 Drug development

    Antisense oligonucleotides (ASOs) are promising therapeutic agents for a variety of neurodegenerative and neuromuscular disorders, e.g., Alzheimer's, Parkinson's and Huntington's diseases, spinal muscular atrophy (SMA) and amyotrophic lateral sclerosis (ALS), caused by genetic abnormalities or increased protein accumulation.

  7. Targeting Amyloid-β Precursor Protein, APP, Splicing with Antisense Oligonucleotides Reduces Toxic Amyloid-β Production

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Molecular therapy : the journal of the American Society of Gene Therapy 2018-03-06 Drug development

    Alterations in amyloid beta precursor protein (APP) have been implicated in cognitive decline in Alzheimer's disease (AD), which is accelerated in Down syndrome/Trisomy 21 (DS/TS21), likely due to the extra copy of the APP gene, located on chromosome 21.

  8. Peripheral Administration of GSK-3β Antisense Oligonucleotide Improves Learning and Memory in SAMP8 and Tg2576 Mouse Models of Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of Alzheimer's disease : JAD 2016-10-01 Drug development

    Glycogen synthase kinase (GSK)-3β is a multifunctional protein that has been implicated in the pathological characteristics of Alzheimer's disease (AD), including the heightened levels of neurofibrillary tangles, amyloid-beta (Aβ), and neurodegeneration.

  9. A Tandem Oligonucleotide Approach for SNP-Selective RNA Degradation Using Modified Antisense Oligonucleotides

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. PloS one 2015-11-06 Drug development

    Antisense oligonucleotides have been studied for many years as a tool for gene silencing.

  10. Direct intracerebral delivery of a miR-33 antisense oligonucleotide into mouse brain increases brain ABCA1 expression. [Corrected]

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuroscience letters 2015-05-06 Drug development

    The ATP-binding cassette transporter A1 (ABCA1) is a membrane bound protein that serves to efflux cholesterol and phospholipids onto lipid poor apolipoproteins during HDL biogenesis.

  11. Antisense oligonucleotide therapy for the treatment of C9ORF72 ALS/FTD diseases

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Molecular neurobiology 2014-05-09 Drug development

    Motor neuron disorders, and particularly amyotrophic lateral sclerosis (ALS), are fatal diseases that are due to the loss of motor neurons in the brain and spinal cord, with progressive paralysis and premature death.

  12. Central and peripheral administration of antisense oligonucleotide targeting amyloid-β protein precursor improves learning and memory and reduces neuroinflammatory cytokines in Tg2576 (AβPPswe) mice

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of Alzheimer's disease : JAD 2014-01-01 Drug development

    Alzheimer's disease (AD) is a progressive neurodegenerative disease.

  13. Peripheral administration of antisense oligonucleotides targeting the amyloid-β protein precursor reverses AβPP and LRP-1 overexpression in the aged SAMP8 mouse brain

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of Alzheimer's disease : JAD 2012-01-01 Drug development

    The senescence accelerated mouse-prone 8 (SAMP8) mouse model of Alzheimer's disease has a natural mutation leading to age-related increases in the amyloid-β protein precursor (AβPP) and amyloid-β (Aβ) in the brain, memory impairment, and deficits in Aβ removal from the brain.

  14. Suppression of choroid plexus transthyretin levels by antisense oligonucleotide treatment

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis 2010-06-01 Drug development

    Leptomeningeal amyloidosis associated with mutations in transthyretin (TTR) is a rare but fatal form of amyloidosis.

  15. Proteomic identification of less oxidized brain proteins in aged senescence-accelerated mice following administration of antisense oligonucleotide directed at the Abeta region of amyloid precursor protein

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Brain research. Molecular brain research 2005-07-01 Drug development

    Amyloid beta-peptide (Abeta) is the major constituent of senile plaques, a pathological hallmark of Alzheimer's disease (AD) brain.

  16. Modulation of the PC12 cell response to nerve growth factor by antisense oligonucleotide to amyloid precursor protein

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Cellular and molecular neurobiology 1994-10-01 Drug development

    1. The amyloid precursor protein (APP) is widely distributed among eukaryotic cells, however, its precise role in cellular functioning is not fully clarified.

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