ReviewCell communication and signaling : CCS2014
Signaling pathway cross talk in Alzheimer's disease.
Review in Cell communication and signaling : CCS, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 2 of them syntheses 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
70 citing papers in PubMed, 2 syntheses or guidelines pooled it, 164 citations in OpenAlex.
- Evidence and Therapeutic Perspectives in the Relationship between the Oral Microbiome and Alzheimer's Disease: A Systematic Review.International journal of environmental research and public health · 2021Pooled it
- A Meta-Analysis of Alzheimer's Disease Brain Transcriptomic Data.Journal of Alzheimer's disease : JAD · 2019Pooled it
- Peroxisome proliferator-activated receptor gamma (PPARγ) as a mechano-metabolic transducer: coordinating lipid homeostasis through mechanical cues.Molecular biomedicine · 2026Review
- SIEVEseq: unified differential expression, variability, and skewness analyses using RNA-Seq data.DNA research : an international journal for rapid publication of reports on genes and genomes · 2026Article
- BioMedGraphica: an all-in-one platform for joint textual biomedical prior knowledge and numeric graph generation.Bioinformatics (Oxford, England) · 2026Article
- Tracing the threads: How toxic metals contribute to neurodegeneration.IBRO neuroscience reports · 2026Review
- Heteroaggregation of Antimicrobial Peptides LL-37 and HNP‑1 Drives Cooperative Neutralization of Cytotoxicity.JACS Au · 2026Article
- Adipokines at the Metabolic-Brain Interface: Therapeutic Modulation by Antidiabetic Agents and Natural Compounds in Alzheimer's Disease.Pharmaceuticals (Basel, Switzerland) · 2025Review
- BioMedGraphica: An All-in-One Platform for Joint Textual Biomedical Prior Knowledge and Numeric Graph Generation.bioRxiv : the preprint server for biology · 2025Article
- Article
- Research Progress on the Interaction Between SIRT1 and Mitochondrial Biochemistry in the Aging of the Reproductive System.Biology · 2025Review
- Evaluation of altered cell-cell communication between glia and neurons in the hippocampus of 3xTg-AD mice at two time points.Journal of cell communication and signaling · 2025Article
- Advancements in nose-to-brain drug targeting for Alzheimer's disease: a review of nanocarriers and clinical insights.Inflammopharmacology · 2025Review
- Unraveling the molecular basis of snake venom nerve growth factor: human TrkA recognition through molecular dynamics simulation and comparison with human nerve growth factor.Frontiers in bioinformatics · 2025Article
- The pathophysiology of mixed Alzheimer's disease and vascular dementia.Theranostics · 2025Review
- Evaluation of altered cell-cell communication between glia and neurons in the hippocampus of 3xTg-AD mice at two time points.bioRxiv : the preprint server for biology · 2024Article
- Recent advances in Alzheimer's disease: Mechanisms, clinical trials and new drug development strategies.Signal transduction and targeted therapy · 2024Review
- Multifaceted neuroprotective approach of Trolox in Alzheimer's disease mouse model: targeting Aβ pathology, neuroinflammation, oxidative stress, and synaptic dysfunction.Frontiers in cellular neuroscience · 2024Article
- Simple model systems reveal conserved mechanisms of Alzheimer's disease and related tauopathies.Molecular neurodegeneration · 2023Review
- Assessment of tau phosphorylation and β-amyloid pathology in human drug-resistant epilepsy.Epilepsia open · 2023Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Numerous studies suggest energy failure and accumulative intracellular waste play a causal role in the pathogenesis of several neurodegenerative disorders and Alzheimer's disease (AD) in particular. AD is characterized by extracellular amyloid deposits, intracellular neurofibrillary tangles, cholinergic deficits, synaptic loss, inflammation and extensive oxidative stress. These pathobiological changes are accompanied by significant behavioral, motor, and cognitive impairment leading to accelerated mortality. Currently, the potential role of several metabolic pathways associated with AD, including Wnt signaling, 5' adenosine monophosphate-activated protein kinase (AMPK), mammalian target of rapamycin (mTOR), Sirtuin 1 (Sirt1, silent mating-type information regulator 2 homolog 1), and peroxisome proliferator-activated receptor gamma co-activator 1-α (PGC-1α) have widened, with recent discoveries that they are able to modulate several pathological events in AD. These include reduction of amyloid-β aggregation and inflammation, regulation of mitochondrial dynamics, and increased availability of neuronal energy. This review aims to highlight the involvement of these new set of signaling pathways, which we have collectively termed "anti-ageing pathways", for their potentiality in multi-target therapies against AD where cellular metabolic processes are severely impaired.
Indexed as
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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.