ArticleBrain, behavior, & immunity - health2025
Leptin and inflammatory pathways in the Alzheimer's disease continuum: Implications for glial activation and neuropsychiatric symptoms.
Article in Brain, behavior, & immunity - health, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Neuroprotective effects of ursodeoxycholic acid in Parkinson's disease and Alzheimer's disease.Neuroprotection (Chichester, England) · 2026Review
- Leptin as a Potential Modifier of Neuroinflammation: Contrasting Roles in Alzheimer's Disease and Multiple Sclerosis.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
18 authors.
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Abstract
Introduction: Chronic peripheral inflammation triggered by adipokine release may extend to the brain, potentially influencing the pathological progression of Alzheimer's disease (AD) and neuropsychiatric symptoms (NPS). However, it remains unclear whether and how leptin contributes to the link between adipose tissue dysfunction and dementia. This study aims to investigate the role of leptin in the connection between adipose-derived inflammatory signaling and cognitive impairment/NPS. Methods: Path analysis was employed to explore how leptin relates to the association between adipose-related metabolic dysfunction and dementia through inflammatory pathways in patients with AD pathology (n = 15). Variables included plasma leptin concentration, body mass index (BMI) as a marker of adiposity, and in vivo assessments of regional neuroinflammation using translocator protein (TSPO)-PET imaging with the tracer Results: Regression analysis demonstrated that higher plasma leptin concentrations positively correlated with BMI and significantly predicted Discussion: These findings underscore the relevance of exploring how leptin and adipose tissue dysfunction interact with neuroinflammatory processes in contributing to NPS in the patients in the AD continuum. Interventions targeting these interactions could represent promising avenues for managing NPS.
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