ReviewMolecular neurobiology2018
Synaptic Dysfunction in Alzheimer's Disease: Aβ, Tau, and Epigenetic Alterations.
Review in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 124 citations in OpenAlex.
- The Association Between Folate and Alzheimer's Disease: A Systematic Review and Meta-Analysis.Frontiers in neuroscience · 2021Pooled it
- A massively parallel CRISPR-based screening platform for modifiers of neuronal depolarization.Nature communications · 2026Article
- Nanoparticles in Vascular Dementia: Advantages and Challenges.CNS neuroscience & therapeutics · 2026Review
- Sovateltide at the heart-brain axis crosstalk in Alzheimer's disease: a promising multi-target and cutting-edge therapeutic approach.Inflammopharmacology · 2026Review
- Synaptic aging and neurodegeneration: the role of synaptic vesicle dynamics and neurotransmitter imbalance.Biogerontology · 2026Review
- Mechanism of Tiaogeng decoction in a cognitive dysfunction mouse model.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Pathological mechanisms and treatment progression of Alzheimer's disease.European journal of medical research · 2025Review
- CRISPR/Cas9 and iPSC-Based Therapeutic Approaches in Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2025Review
- Aging-dependent YAP1 reduction contributes to AD pathology by upregulating the Nr4a1-AKT/GSK-3β axis.Translational neurodegeneration · 2025Article
- Chronic Vanadium Exposure Promotes Aggregation of Alpha-Synuclein, Tau and Amyloid Beta in Mouse Brain.Journal of neurochemistry · 2025Article
- Dynamic and Static Structure-Function Coupling With Machine Learning for the Early Detection of Alzheimer's Disease.Human brain mapping · 2025Article
- Integration of phytochemical profiling and computational approaches to evaluate the neuroprotective potential ofBiotechnology reports (Amsterdam, Netherlands) · 2025Article
- Article
- Editorial: Current chemical approaches in combating neuroinflammation in Alzheimer's disease (AD).Frontiers in aging neuroscience · 2025Article
- Neurodegeneration in the cortical sulcus is a feature of chronic traumatic encephalopathy and associated with repetitive head impacts.Acta neuropathologica · 2024Article
- Autophagy in Disease Onset and Progression.Aging and disease · 2024Review
- Stepwise Structural Simplification of the Dihydroxyanthraquinone Moiety of a Multitarget Rhein-Based Anti-Alzheimer Lead to Improve Drug Metabolism and Pharmacokinetic Properties.Pharmaceutics · 2024Article
- Delivering synaptic protein mRNAs via extracellular vesicles ameliorates cognitive impairment in a mouse model of Alzheimer's disease.BMC medicine · 2024Article
- Hepatotoxicity assessment of innovative nutritional supplements based on olive-oil formulations enriched with natural antioxidants.Frontiers in nutrition · 2024Article
- Association between Alzheimer's disease pathologic products and age and a pathologic product-based diagnostic model for Alzheimer's disease.Frontiers in aging neuroscience · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized in the early stages by loss of learning and memory. However, the mechanism underlying these symptoms remains unclear. The best correlation between cognitive decline and pathological changes is in synaptic dysfunction. Histopathological hallmarks of AD are the abnormal aggregation of Aβ and Tau. Evidence suggests that Aβ and Tau oligomers contribute to synaptic loss in AD. Recently, direct links between epigenetic alterations, such as dysfunction in non-coding RNAs (ncRNAs), and synaptic pathologies have emerged, raising interest in exploring the potential roles of ncRNAs in the synaptic deficits in AD. In this paper, we summarize the potential roles of Aβ, Tau, and epigenetic alterations (especially by ncRNAs) in the synaptic dysfunction of AD and discuss the novel findings in this area.
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.