ReviewNeurobiology of disease2022
Glial-neuron crosstalk in health and disease: A focus on metabolism, obesity, and cognitive impairment.
Review in Neurobiology of disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.
- Anti-obesity medications and cognitive disorder risk: a discrepancy between RCTs and real-world evidence.Frontiers in pharmacology · 2026Pooled it
- Effects of obesity on brain health and cognition.Nature reviews. Neurology · 2026Review
- Multi-Omics Mendelian Randomization Maps Lipid-Related Brain Cell-Type Associations with Kidney Disease.Genes · 2026Article
- Diabetes and the Metabolic Syndrome as Drivers of Neurodegeneration: Convergent Mechanisms Linking Peripheral Neuropathy and Dementia.Annals of neurology · 2026Review
- Tmem117, an oligodendrocyte-enriched regulator of NCX activity, links myelin homeostasis to counterregulation and metabolic health.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Potential role of PPAR-γ/MCT1-related mechanisms in INT131-mediated protection against chronic stress-induced neurobehavioral dysfunction.Psychopharmacology · 2026Article
- Neuroinflammation in Alzheimer's and Parkinson's diseases: pathogenic mechanisms and therapeutic strategies.Translational neurodegeneration · 2026Review
- Obesity-Related Cognitive Impairment: An Update Overview of Mechanisms and Treatments.Expert reviews in molecular medicine · 2026Review
- Dietary Choline and Betaine Intake and 2-year Changes in Cognitive Function in Older Adults With Overweight or Obesity and Metabolic Syndrome: A Prospective Cohort Analysis.The American journal of clinical nutrition · 2026Article
- Enriched Environment Suppresses Neuronal Ferroptosis Through SIRT1/AKT/GSK3β-Dependent Glycogen Metabolic Reprogramming After Cerebral Ischemia-Reperfusion.Antioxidants (Basel, Switzerland) · 2026Article
- Energetic diversity in retinal ganglion cells is modulated by neuronal activity and correlates with resilience to degeneration.Nature communications · 2026Article
- The metabolic roots of memory loss: interlinking the Diabetes-Alzheimer's hypothesis.Metabolic brain disease · 2026Review
- Cholinergic Phenotypes of Acetyl-CoA with ATP-Citrate Lyase Link.International journal of molecular sciences · 2026Review
- Hijacking Sodium-Glucose Cotransporters: Fructose Drives Neuronal and Microglial Dysfunction.ASN neuro · 2026Article
- ApoE expression across the CNS: Who, What, Where, When, and How (much)?Molecular neurodegeneration advances · 2026Review
- Article
- Are we giving too much weight to lean mass loss?Molecular metabolism · 2025Review
- Role of astrocytes in diabetic neuropathy: Review of their involvement in disease mechanisms.World journal of diabetes · 2025Review
- A Neural-Glial Model of the ApoE-SORT1-FABP7 Axis Tied to Sleep Disruption and Alzheimer's Disease Pathophysiology.Biomolecules · 2025Review
- Porphyromonas gingivalis promotes the formation and development of type 2 diabetes mellitus complicated with cognitive impairment by regulating gut microbiota and metabolic pathways.Molecular medicine (Cambridge, Mass.) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Dementia is a complex set of disorders affecting normal cognitive function. Recently, several clinical studies have shown that diabetes, obesity, and components of the metabolic syndrome (MetS) are associated with cognitive impairment, including dementias such as Alzheimer's disease. Maintaining normal cognitive function is an intricate process involving coordination of neuron function with multiple brain glia. Well-orchestrated bioenergetics is a central requirement of neurons, which need large amounts of energy but lack significant energy storage capacity. Thus, one of the most important glial functions is to provide metabolic support and ensure an adequate energy supply for neurons. Obesity and metabolic disease dysregulate glial function, leading to a failure to respond to neuron energy demands, which results in neuronal damage. In this review, we outline evidence for links between diabetes, obesity, and MetS components to cognitive impairment. Next, we focus on the metabolic crosstalk between the three major glial cell types, oligodendrocytes, astrocytes, and microglia, with neurons under physiological conditions. Finally, we outline how diabetes, obesity, and MetS components can disrupt glial function, and how this disruption might impair glia-neuron metabolic crosstalk and ultimately promote cognitive impairment.
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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.