International review of neurobiologyJul 13, 2026

Insulin resistance and obesity as key causes of energy problems in Alzheimer's disease

Gut-Brain Axis Weekly Brief ↗PubMed ↗DOI ↗

Updated Jul 14, 2026

Abstract

Alzheimer's disease is associated with profound disturbances in brain energy metabolism.

Insulin resistance and obesity may contribute significantly to metabolic dysfunction in Alzheimer's disease.
Impaired insulin signaling, excess body fat, and cognitive decline are interconnected.
Obesity-related inflammation and imbalances in fat cell signals could accelerate insulin resistance in the brain.
Evidence suggests glucose hypometabolism and mitochondrial dysfunction are present in Alzheimer's disease.
Amyloid and tau pathology may result from prolonged energy insufficiency in the brain.
Emerging treatments targeting metabolic restoration could serve as potential strategies for modifying Alzheimer's disease.

Simplified

Alzheimer's disease (AD) is increasingly recognized as a disorder driven not only by classical neuropathological hallmarks but also by profound disturbances in brain energy metabolism. Growing evidence points to insulin resistance and obesity as major contributors to this metabolic crisis, linking peripheral metabolic dysfunction to central neurodegenerative processes. This chapter explores AD in the light of bioenergetic failure, highlighting the epidemiological and mechanistic connections between impaired insulin signaling, excess adiposity, and cognitive decline. The chapter further highlights how obesity-related inflammation, adipokine imbalance, and gut-brain axis dysregulation accelerates central insulin resistance and neuronal vulnerability. Evidence for glucose hypometabolism, mitochondrial failure, and disrupted astrocyte-neuron metabolic coupling in AD is reviewed, positioning amyloid and tau pathology as downstream consequences of sustained energy insufficiency. Finally, emerging therapeutic strategies aimed at restoring metabolic balance ranging from insulin-based interventions to lifestyle and mitochondria-targeted approaches are discussed, underscoring the potential of metabolic restoration as a disease-modifying strategy in Alzheimer's disease.

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Insulin resistance and obesity as key causes of energy problems in Alzheimer's disease

Abstract

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