Antisense oligonucleotides for Alzheimer's disease therapy: from the mRNA to miRNA paradigm
Open Access
- 10 November 2021
- journal article
- research article
- Published by Elsevier in EBioMedicine
- Vol. 74, 103691
Abstract
No abstract availableKeywords
Funding Information
- Horizon 2020 (3548/H2020/COFUND/2016/2, 737390)
- European Commission
- National Science Centre Poland
- Ministerstwo Edukacji i Nauki
This publication has 90 references indexed in Scilit:
- Transition of a microRNA from Repressing to Activating Translation Depending on the Extent of Base Pairing with the TargetPLOS ONE, 2013
- 95. Antisense directed against the amyloid precursor protein reduces cytokine expression in the brain and improves learning and memory in the Tg2576 mouse model of Alzheimer’s diseaseBrain, Behavior, and Immunity, 2012
- miR‐206 regulates brain‐derived neurotrophic factor in Alzheimer disease modelAnnals of Neurology, 2012
- Highly Efficient miRNA-Mediated Reprogramming of Mouse and Human Somatic Cells to PluripotencyCell Stem Cell, 2011
- MicroRNA-101 downregulates Alzheimer’s amyloid-β precursor protein levels in human cell cultures and is differentially expressedBiochemical and Biophysical Research Communications, 2011
- New class of microRNA targets containing simultaneous 5′-UTR and 3′-UTR interaction sitesGenome Research, 2009
- Most mammalian mRNAs are conserved targets of microRNAsGenome Research, 2008
- MicroRNA-10a Binds the 5′UTR of Ribosomal Protein mRNAs and Enhances Their TranslationMolecular Cell, 2008
- Antisense inhibition at the β-secretase-site of β-amyloid precursor protein reduces cerebral amyloid and acetyl cholinesterase activity in Tg2576Neuroscience, 2007
- Antisense oligonucleotide therapy for neurodegenerative diseaseJournal of Clinical Investigation, 2006