ReviewFrontiers in endocrinology2024
Therapeutic targeting of obesity-induced neuroinflammation and neurodegeneration.
Review in Frontiers in endocrinology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed.
- Palmitic acid-induced autolysosomal dysfunction and lipotoxicity in neuroinflammation and neurodegeneration.Neural regeneration research · 2026Article
- Microbiota-Gut-Brain Axis Disruption, Neuroinflammation, and Potential Antioxidant-Based Treatments in Metabolic Diseases.Antioxidants (Basel, Switzerland) · 2026Review
- Article
- Neurometabolic and Neuroinflammatory Consequences of Obesity: Insights into Brain Vulnerability and Imaging-Based Biomarkers.International journal of molecular sciences · 2026Review
- Is Obesity a Modifiable Risk Factor in Multiple Sclerosis? Mechanistic Insights into Neuroinflammation and Oxidative Damage.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- Obesity-induced cofilin1 pathway dysregulation: Possible molecular links between neuroinflammation, cognitive decline, and Alzheimer's disease biomarkers.IBRO neuroscience reports · 2025Article
- TNF as a mediator of metabolic inflammation and body-brain interaction in obesity-driven neuroinflammation and neurodegeneration.Ageing research reviews · 2025Review
- The orexin/hypocretin system in dementia-related neurological disorders: a double-edged sword in cognitive impairment.Psychopharmacology · 2025Review
- Autolysosomal Dysfunction in Obesity-induced Metabolic Inflammation and Related Disorders.Current obesity reports · 2025Review
- Energy Metabolism and Brain Aging: Strategies to Delay Neuronal Degeneration.Cellular and molecular neurobiology · 2025Review
- Lysosomal acidification impairment in astrocyte-mediated neuroinflammation.Journal of neuroinflammation · 2025Review
- Probiotic attributes and safety profile of AKM Lab-01: a novelFrontiers in microbiology · 2025Article
- What role will physiological resilience play in brown-white fat dynamic in obesity management?Frontiers in pharmacology · 2025Article
- Therapeutic targets in diabetic peripheral neuropathy: heat shock proteins.Frontiers in endocrinology · 2025Review
- A unique polygenic mouse model of obesity exhibits a distinct immunological profile that may offer protection against systemic inflammation, diabetes, and behavioral impairments.Frontiers in immunology · 2025Article
- Targeting the inter-monomeric space of TNFR1 pre-ligand dimers: A novel binding pocket for allosteric modulators.Computational and structural biotechnology journal · 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity is a major modifiable risk factor leading to neuroinflammation and neurodegeneration. Excessive fat storage in obesity promotes the progressive infiltration of immune cells into adipose tissue, resulting in the release of pro-inflammatory factors such as cytokines and adipokines. These inflammatory mediators circulate through the bloodstream, propagating inflammation both in the periphery and in the central nervous system. Gut dysbiosis, which results in a leaky intestinal barrier, exacerbates inflammation and plays a significant role in linking obesity to the pathogenesis of neuroinflammation and neurodegeneration through the gut-brain/gut-brain-liver axis. Inflammatory states within the brain can lead to insulin resistance, mitochondrial dysfunction, autolysosomal dysfunction, and increased oxidative stress. These disruptions impair normal neuronal function and subsequently lead to cognitive decline and motor deficits, similar to the pathologies observed in major neurodegenerative diseases, including Alzheimer's disease, multiple sclerosis, and Parkinson's disease. Understanding the underlying disease mechanisms is crucial for developing therapeutic strategies to address defects in these inflammatory and metabolic pathways. In this review, we summarize and provide insights into different therapeutic strategies, including methods to alter gut dysbiosis, lifestyle changes, dietary supplementation, as well as pharmacological agents derived from natural sources, that target obesity-induced neuroinflammation and neurodegeneration.
Indexed as
Identifiers
What Socratic 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 Socratic graph.