ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2024
Suppressing UBE2N ameliorates Alzheimer's disease pathology through the clearance of amyloid beta.
Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Integrated single-cell and bulk transcriptomic analyses reveal cDC1-centered ubiquitination dysregulation and identify UBE2F as a critical regulator in sepsis.Frontiers in immunology · 2026Article
- Inhibition of UBE2N promotes the clearance of mutant HTT (huntingtin) in HD knock-in mice.Autophagy · 2025Article
- SIK2-mediated phosphorylation of GABARAPL2 facilitates autophagosome-lysosome fusion and rescues neurodegeneration in an Alzheimer's disease model.Translational neurodegeneration · 2025Article
- Label-Free Proteomic Profiling of the dvls2 (CL2006) Caenorhabditis elegans Alzheimer's Disease (AD) Model Reveals Conserved Molecular Signatures Shared With the Human AD Brain.Journal of neurochemistry · 2025Article
- Spotlight on Alzheimer's disease and related dementias research in East Asia.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Ubiquitin-proteasome system in the different stages of dominantly inherited Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Intranasal Delivery of Brain-Derived Neurotrophic Factor (BDNF)-Loaded Small Extracellular Vesicles for Treating Acute Spinal Cord Injury in Rats and Monkeys.Journal of extracellular vesicles · 2025Article
- Suppressing UBE2N ameliorates Alzheimer's disease pathology through the clearance of amyloid beta.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Ubiquitin-Proteasome System in the Different Stages of Dominantly Inherited Alzheimer's Disease.Research square · 2024Article
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15 authors.
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Abstract
introductionAging is one of the risk factors for the early onset of Alzheimer's disease (AD). We previously discovered that the age-dependent increase in Ubiquitin Conjugating Enzyme E2 N (UBE2N) plays a role in the accumulation of misfolded proteins through K63 ubiquitination, which has been linked to AD pathogenesis. However, the impact of UBE2N on amyloid pathology and clearance has remained unknown.
resultsWe observed the elevated UBE2N during the amyloid beta (Aβ) generation in the brains of 5×FAD, APP/PS1 mice, and patients with AD, in comparison to healthy individuals. UBE2N overexpression exacerbated amyloid deposition in 5×FAD mice and senescent monkeys, whereas knocking down UBE2N via CRISPR/Cas9 reduced Aβ generation and cognitive deficiency. Moreover, pharmacological inhibition of UBE2N ameliorated Aβ pathology and subsequent transcript defects in 5×FAD mice. DISCUSSION: We have discovered that age-dependent expression of UBE2N is a critical regulator of AD pathology. Our findings suggest that UBE2N could serve as a potential pharmacological target for the advancement of AD therapeutics. HIGHLIGHTS: Ubiquitin Conjugating Enzyme E2 N (UBE2N) level was elevated during amyloid beta (Aβ) deposition in AD mouse and patients' brains. UBE2N exacerbated Aβ generation in the AD mouse and senescent monkey. Drug inhibition of UBE2N ameliorated Aβ pathology and cognitive deficiency.
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