ReviewMetabolites2023
Obesity-Induced Brain Neuroinflammatory and Mitochondrial Changes.
Review in Metabolites, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.
- Vascular risk factors for idiopathic normal pressure hydrocephalus: a systematic review and meta-analysis.Frontiers in neurology · 2023Pooled it
- Exercise attenuates obesity-related cognitive and sleep-circadian dysfunctions by attenuating neuroinflammation via JAK/STAT in sex and age specific manner.International journal of obesity (2005) · 2026Article
- Multimorbidity burden and patterns associated with DeepBrainNet-derived brain-age gap in dementia-free older adults: A community-based study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Prefrontal Cortex Dysregulation of Amino Acid-Glucose Homeostasis Links High-Fat and/or High-Fructose Intake to Cognitive Deficits in Male Mice.Neurochemical research · 2026Article
- Visceral adipose tissue differentially affects tau and Aβ pathology in 3xTg-AD mice.Cell communication and signaling : CCS · 2026Article
- Complement 3a Receptor mediates high fat diet induced hypothalamic accumulation of lipid associated microglia to regulate neuroinflammation and obesity.bioRxiv : the preprint server for biology · 2026Article
- The alteration of brain function in overweight/obese individuals and the neurological benefit of thymoquinone: uncovering molecular mechanisms.Metabolic brain disease · 2026Review
- Obesity supersizes macrophage and neutrophil activation after stroke while lipid droplets play a protective role.Journal of neuroinflammation · 2026Article
- The Regulatory Role of FABP4 in Microbiome-Brain-Gut Communication Under High-Fat-Diet Conditions.International journal of molecular sciences · 2026Review
- Precision nutrition in weight loss and neuroendocrine control of people with obesity: The study protocol of a factorial randomised controlled trial (GenON Programme).Diabetes, obesity & metabolism · 2026Article
- Obesity-induced cognitive impairment: Underlying mechanisms and therapeutic prospects.Metabolism open · 2026Review
- Novel mechanism of neuronal hypoxia response: HIF-1α/STOML2 mediated PINK1-dependent mitophagy activation against neuronal injury.Cell death discovery · 2026Article
- Article
- Elevated body roundness index and epilepsy prevalence: a cross-sectional study.Scientific reports · 2026Article
- Metabolic inflammation at the adipose-brain axis.Frontiers in physiology · 2026Review
- Association of weight-adjusted waist index with motoric cognitive risk syndrome in Chinese adults Aged ≥ 60 years.Lipids in health and disease · 2025Article
- Adipose Tissue and Central Nervous System Crosstalk: Roles in Pain and Cognitive Dysfunction.Biomedicines · 2025Review
- Evaluation ofMetabolites · 2025Article
- Oxidative Stress, Antioxidant Cofactor Micronutrients, and Cognitive Outcomes in Childhood Obesity: Mechanisms, Evidence, and Therapeutic Opportunities.International journal of molecular sciences · 2025Review
- Obesity Hacks the Brain's Systems for Weight Loss Resistance.Molecular neurobiology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Obesity is defined as abnormal and excessive fat accumulation, and it is a risk factor for developing metabolic and neurodegenerative diseases and cognitive deficits. Obesity is caused by an imbalance in energy homeostasis resulting from increased caloric intake associated with a sedentary lifestyle. However, the entire physiopathology linking obesity with neurodegeneration and cognitive decline has not yet been elucidated. During the progression of obesity, adipose tissue undergoes immune, metabolic, and functional changes that induce chronic low-grade inflammation. It has been proposed that inflammatory processes may participate in both the peripheral disorders and brain disorders associated with obesity, including the development of cognitive deficits. In addition, mitochondrial dysfunction is related to inflammation and oxidative stress, causing cellular oxidative damage. Preclinical and clinical studies of obesity and metabolic disorders have demonstrated mitochondrial brain dysfunction. Since neuronal cells have a high energy demand and mitochondria play an important role in maintaining a constant energy supply, impairments in mitochondrial activity lead to neuronal damage and dysfunction and, consequently, to neurotoxicity. In this review, we highlight the effect of obesity and high-fat diet consumption on brain neuroinflammation and mitochondrial changes as a link between metabolic dysfunction and cognitive decline.
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.