ArticleAging cell2022
Acrolein, an endogenous aldehyde induces synaptic dysfunction in vitro and in vivo: Involvement of RhoA/ROCK2 pathway.
Article in Aging cell, 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 15 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
15 citing papers in PubMed, 26 citations in OpenAlex.
- A Niacin-α-Lipoic Acid Hybrid Ameliorates Alzheimer's Disease Pathology in Mouse Models.ACS pharmacology & translational science · 2026Article
- Esketamine Alleviates Postoperative Cognitive Dysfunction via Rock2/Add1 Signaling Pathway in Aged Mice.Neurochemical research · 2026Article
- Serum butyraldehyde levels are associated with abdominal aortic calcification: a population-based study.European journal of medical research · 2026Article
- Structural Isomer Cumulative molecular fingerprinting method (SIC) for standardizing structural isomeric relationships.Communications chemistry · 2025Article
- Acrolein-Induced Alterations in Morphology and Stress Resilience in hiPSC-Derived Cortical Neurons.Environmental science & technology · 2025Article
- Impairment of Tricarboxylic Acid Cycle (TCA) Cycle in Alzheimer's Disease: Mechanisms, Implications, and Potential Therapies.Aging and disease · 2025Review
- Exploring the Role of RhoA/ROCK Signaling in Pain: A Narrative Review.Aging and disease · 2025Review
- Pre-electroacupuncture Ameliorates Cerebral Ischemia-reperfusion Injury by Inhibiting Microglial RhoA/pyrin/GSDMD Signaling Pathway.Neurochemical research · 2024Article
- Investigating the association between the GAP-43 concentration with diffusion tensor imaging indices in Alzheimer's dementia continuum.BMC neurology · 2024Article
- Sevoflurane-induced overexpression of extrasynaptic α5-GABAAging cell · 2024Article
- A comprehensive bibliometric analysis of global research on the role of acrolein in Alzheimer's disease pathogenesis: involvement of amyloid-beta.Frontiers in aging neuroscience · 2024Article
- Role of Rho-associated kinases and their inhibitor fasudil in neurodegenerative diseases.Frontiers in neuroscience · 2024Review
- Insight into the emerging and common experimental in-vivo models of Alzheimer's disease.Laboratory animal research · 2023Review
- Molecular Characteristics of Toxicity of Acrolein Produced from Spermine.Biomolecules · 2023Review
- Acrolein, an endogenous aldehyde induces synaptic dysfunction in vitro and in vivo: Involvement of RhoA/ROCK2 pathway.Aging cell · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acrolein, an unsaturated aldehyde, is increased in the brain of Alzheimer's disease (AD) patients and identified as a potential inducer of sporadic AD. Synaptic dysfunction, as a typical pathological change occurring in the early stage of AD, is most closely associated with the severity of dementia. However, there remains a lack of clarity on the mechanisms of acrolein inducing AD-like pathology and synaptic impairment. In this study, acrolein-treated primary cultured neurons and mice were applied to investigate the effects of acrolein on cognitive impairment and synaptic dysfunction and their signaling mechanisms. In vitro, ROCK inhibitors, Fasudil, and Y27632, could attenuate the axon ruptures and synaptic impairment caused by acrolein. Meanwhile, RNA-seq distinct differentially expressed genes in acrolein models and initially linked activated RhoA/Rho-kinase2 (ROCK2) to acrolein-induced synaptic dysfunction, which could regulate neuronal cytoskeleton and neurite. The Morris water maze test and in vivo field excitatory postsynaptic potential (fEPSP) were performed to evaluate spatial memory and long-term potential (LTP), respectively. Acrolein induced cognitive impairment and attenuated LTP. Furthermore, the protein level of Synapsin 1 and postsynaptic density 95 (PSD95) and dendritic spines density were also decreased in acrolein-exposed mice. These changes were improved by ROCK2 inhibitor Fasudil or in ROCK2
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.