ArticleNature communications2022
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Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026Review
- Gut microbiota as a modulator of HDAC: insights into Alzheimer's disease treatment.Pharmacological reports : PR · 2026Review
- Imaging brain class I histone deacetylase changes in the Lewy body dementias and Parkinson's disease.Clinical epigenetics · 2026Article
- Premature aging in serious mental illness.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Review
- Can Nuclear Imaging Detect Trained Immunity in Cardiovascular Disease?Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Intepirdine Derivatives Possessing Dual 5HT6 Antagonism / HDAC6 Inhibitory Activity.Chemistry (Weinheim an der Bergstrasse, Germany) · 2025Article
- Histone Deacetylases in Neurodegenerative Diseases and Their Potential Role as Therapeutic Targets: Shedding Light on Astrocytes.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Review
- Martinostat as a novel HDAC inhibitor to overcome tyrosine kinase inhibitor resistance in chronic myeloid leukemia.Clinical epigenetics · 2025Article
- Histone Deacetylase 6 Brain PET in Amyotrophic Lateral Sclerosis-Frontotemporal Spectrum Disorder.Annals of clinical and translational neurology · 2025Article
- Histone Deacetylation in Alzheimer's Diseases (AD); Hope or Hype.Cell biochemistry and biophysics · 2025Review
- The impact of sex on memory during aging and Alzheimer's disease progression: Epigenetic mechanisms.Journal of Alzheimer's disease : JAD · 2024Review
- Toward AI-driven neuroepigenetic imaging biomarker for alcohol use disorder: A proof-of-concept study.iScience · 2024Article
- Epigenetics of Fear, Anxiety and Stress - Focus on Histone Modifications.Current neuropharmacology · 2024Article
- Aging imaging: the future demand of health management.European journal of nuclear medicine and molecular imaging · 2023Article
- Article
- The use of neuroimaging techniques in the early and differential diagnosis of dementia.Molecular psychiatry · 2023Review
- Reduction of class I histone deacetylases ameliorates ER-mitochondria cross-talk in Alzheimer's disease.Aging cell · 2023Article
- Advances in PET/CT Imaging for Breast Cancer.Journal of clinical medicine · 2023Review
- Transcriptome analysis identifies the role of Class I histone deacetylase in Alzheimer's disease.Heliyon · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
37 authors at 4 institutions in 3 countries.
Funding
Abstract
Alzheimer's disease (AD) is characterized by the brain accumulation of amyloid-β and tau proteins. A growing body of literature suggests that epigenetic dysregulations play a role in the interplay of hallmark proteinopathies with neurodegeneration and cognitive impairment. Here, we aim to characterize an epigenetic dysregulation associated with the brain deposition of amyloid-β and tau proteins. Using positron emission tomography (PET) tracers selective for amyloid-β, tau, and class I histone deacetylase (HDAC I isoforms 1-3), we find that HDAC I levels are reduced in patients with AD. HDAC I PET reduction is associated with elevated amyloid-β PET and tau PET concentrations. Notably, HDAC I reduction mediates the deleterious effects of amyloid-β and tau on brain atrophy and cognitive impairment. HDAC I PET reduction is associated with 2-year longitudinal neurodegeneration and cognitive decline. We also find HDAC I reduction in the postmortem brain tissue of patients with AD and in a transgenic rat model expressing human amyloid-β plus tau pathology in the same brain regions identified in vivo using PET. These observations highlight HDAC I reduction as an element associated with AD pathophysiology.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.