Metabolic inflammation at the adipose-brain axis

Area of Science:

• Neuroscience
• Endocrinology
• Immunology
• Metabolic Disorders

Background:

• Obesity is a global health crisis linked to central nervous system (CNS) dysfunction.
• White adipose tissue (WAT) acts as an endocrine organ, releasing inflammatory mediators during obesity.
• These peripheral signals affect brain physiology, including the blood-brain barrier (BBB) and clearance pathways.

Purpose of the Study:

• To review how obesity-induced changes in white adipose tissue impact brain function.
• To explore the role of adipokines in mediating adipose-brain communication.
• To discuss therapeutic strategies targeting the adipose-brain axis for CNS dysfunction.

Main Methods:

• Review of existing literature on obesity, adipose tissue, and CNS function.
• Analysis of the mechanisms by which peripheral signals affect brain interfaces.
• Examination of the role of specific adipokines (leptin, adiponectin, resistin) in neuroinflammation.

Main Results:

• Obesity promotes neuroinflammation via BBB disruption, impaired clearance, and glial activation.
• Adipokines like leptin, adiponectin, and resistin play key roles in linking metabolic stress to neurodegeneration.
• Sex-dependent vulnerabilities in obesity-associated neuroinflammation are increasingly recognized.

Conclusions:

• The adipose-brain axis is a critical pathway linking metabolic dysfunction to CNS disorders.
• Therapeutic interventions targeting this axis, including lifestyle changes and medications, show promise.
• Further research integrating barrier biology and neuroimmune mechanisms is needed, especially for novel therapies.