ArticleCNS neuroscience & therapeutics2024
Lysine Acetyltransferase TIP60 Restricts Nerve Injury by Activating IKKβ/SNAP23 Axis-Mediated Autophagosome-Lysosome Fusion in Alzheimer's Disease.
Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- HDAC7 acts as an astrocytic mediator of Aβ pathology that directly engages IKK to drive astrocyte neurotoxicity and neurodegeneration in Alzheimer's disease.Alzheimer's research & therapy · 2026Article
- Transcriptional and epigenetic regulation of autophagy: mechanisms, disease relevance and therapeutic opportunities.Signal transduction and targeted therapy · 2026Review
- Study on the improvement effect and mechanism of resveratrol on cognitive impairment in tau mutant adenovirus-induced alzheimer's disease model mice.Psychopharmacology · 2026Article
- Knockdown of SOX4 attenuates sepsis myocardial injury by inhibiting the EZH2/H3K27me3/SOCS3 axis.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Chronic Exercise Protects Against Cognitive Deficits in an Alzheimer's Disease Model by Enhancing Autophagy and Reducing Mitochondrial Abnormalities.Molecular neurobiology · 2025Article
- The Interaction between Oligodendrocytes and Aβ in Alzheimer's Disease.Current Alzheimer research · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
objectiveThe hyperphosphorylation of Tau protein is considered an important cause of neuronal degeneration in Alzheimer's disease (AD). The disruption of neuronal histone acetylation homeostasis mediated by Tip60 HAT is a common early event in neurodegenerative diseases, but the deeper regulatory mechanism on β-amyloid peptide (Aβ)-induced neurotoxicity and autophagic function in AD is still unclear.
methodsAD models were established both in APP/PS1 mice and Aβ
resultsTIP60 overexpression improved cognitive deficits and neurological damage and restored the impairment of autophagy-lysosomes fusion in vivo. Similarly, the upregulation of TIP60 in Aβ
conclusionCollectively, our results highlighted the potential of the TIP60 target for AD and provided new insights into the mechanisms underlying neuroprotection in this disorder.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.