ArticleMolecular neurodegeneration2017
Downregulating ANP32A rescues synapse and memory loss via chromatin remodeling in Alzheimer model.
Article in Molecular neurodegeneration, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- C/EBPβ: A transcription factor associated with the irreversible progression of Alzheimer's disease.CNS neuroscience & therapeutics · 2024Pooled it
- H3K4 Trimethylation Mediate Hyperhomocysteinemia Induced Neurodegeneration via Suppressing Histone Acetylation by ANP32A.Molecular neurobiology · 2024Article
- The Role of Acetylation and Methylation of Rat Hippocampal Histone H3 in the Mechanism of Aluminum-Induced Neurotoxicity.Neurochemical research · 2024Article
- Glaucoma-Associated CDR1 Peptide Promotes RGC Survival in Retinal Explants through Molecular Interaction with Acidic Leucine Rich Nuclear Phosphoprotein 32A (ANP32A).Biomolecules · 2023Article
- Emerging evidence for dysregulated proteome cargoes of tau-propagating extracellular vesicles driven by familial mutations of tau and presenilin.Extracellular vesicles and circulating nucleic acids · 2023Article
- Article
- A Review of the Recent Advances in Alzheimer's Disease Research and the Utilization of Network Biology Approaches for Prioritizing Diagnostics and Therapeutics.Diagnostics (Basel, Switzerland) · 2022Review
- Epigenetics of Alzheimer's Disease.Biomolecules · 2021Review
- STAT3 ameliorates cognitive deficits via regulation of NMDAR expression in an Alzheimer's disease animal model.Theranostics · 2021Article
- The Histone Modifications of Neuronal Plasticity.Neural plasticity · 2021Review
- Tau-induced upregulation of C/EBPβ-TRPC1-SOCE signaling aggravates tauopathies: A vicious cycle in Alzheimer neurodegeneration.Aging cell · 2020Article
- Dysregulation of Exosome Cargo by Mutant Tau Expressed in Human-induced Pluripotent Stem Cell (iPSC) Neurons Revealed by Proteomics Analyses.Molecular & cellular proteomics : MCP · 2020Article
- Article
- Epigenetics of the Synapse in Neurodegeneration.Current neurology and neuroscience reports · 2019Review
- Tau accumulation triggers STAT1-dependent memory deficits by suppressing NMDA receptor expression.EMBO reports · 2019Article
- Bergapten alleviates osteoarthritis by regulating the ANP32A/ATM signaling pathway.FEBS open bio · 2019Article
- Neuropeptide S Ameliorates Cognitive Impairment of APP/PS1 Transgenic Mice by Promoting Synaptic Plasticity and Reducing Aβ Deposition.Frontiers in behavioral neuroscience · 2019Article
- SET de novo frameshift variants associated with developmental delay and intellectual disabilities.European journal of human genetics : EJHG · 2018Article
- Neuron-Specific Menin Deletion Leads to Synaptic Dysfunction and Cognitive Impairment by Modulating p35 Expression.Cell reports · 2018Article
- Oleanolic Acid Ameliorates Aβ25-35 Injection-induced Memory Deficit in Alzheimer's Disease Model Rats by Maintaining Synaptic Plasticity.CNS & neurological disorders drug targets · 2018Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe impairment of histone acetylation is causally linked to the cognitive decline in Alzheimer's disease (AD). In addition to histone acetyltransferases (HATs) and histone deacetylases (HDACs), inhibitor of acetyltransferases (INHAT) can also regulate histone acetylation. As a key component of INHAT, level of ANP32A is selectively upregulated in the brain of AD patients. Here we investigated whether downregulating ANP32A can rescue AD-like synapse and memory deficits.
methodsRFP-labeled lentiviral ANP32A-shRNA was infused stereotaxically into the hippocampal CA3 region of the human tau transgenic mice (termed htau). The spatial learning and memory were assessed by Morris water maze (MWM). The synaptic function was measured by electrophysiological recording and the spine density was detected by Golgi staining. RT-PCR and Western blotting were used to detect the mRNA and protein levels.
resultsElevation of ANP32 in htau transgenic mice was correlated with learning deficits, while the hippocampal infusion of lenti-siANP32A to downregulate ANP32A in 12 m-old htau mice could rescue memory loss. Further studies demonstrated that downregulating ANP32A restored synapse morphology and the function. In the brain of htau mice, the acetylated histone decreased while knockdown ANP32A unmasked histone for a robust acetylation with reduced INHAT complex formation. Downregulating of ANP32A also attenuated AD-like tau hyperphosphorylation. Finally, several AD-associated risk factors, including tau accumulation, β-amyloid and H
conclusionWe conclude that downregulating ANP32A rescues synaptic plasticity and memory ability by reducing INHAT formation and unmasking histone for hyperacetylation. Our findings reveal novel mechanisms for AD memory loss and potential molecular markers for protection.
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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 OpenQuestion graph.