Insulin Sensitivity Neurology is the clinical recognition of the profound impact that peripheral and central nervous system insulin sensitivity has on cognitive function, neuroprotection, and overall brain metabolism. Impaired insulin signaling in the brain, often termed “brain insulin resistance,” is strongly associated with compromised synaptic plasticity, reduced neuronal energy utilization, and increased risk for neurodegenerative processes. Optimization strategies in this domain focus on enhancing the brain’s responsiveness to insulin, thereby improving glucose uptake and utilization by neurons. This link highlights the brain as a metabolically active and hormone-responsive organ.
Origin
This specialized concept emerged from the convergence of endocrinology, which focuses on insulin action, and contemporary neuroscience, particularly research into metabolic dysfunction’s role in neurodegeneration. The term acknowledges the direct presence of insulin receptors on neurons and glial cells, challenging the historical view of the brain as an insulin-independent organ. Its clinical relevance has grown with the recognition of type 3 diabetes as a proposed term for Alzheimer’s disease.
Mechanism
Insulin acts in the central nervous system by binding to neuronal insulin receptors, which then activate signaling pathways crucial for glucose transport, mitochondrial biogenesis, and the regulation of key neurotransmitters. When sensitivity is reduced, these pathways falter, leading to energy deficits and increased oxidative stress within the neurons. Therapeutic approaches aim to restore receptor function and downstream signaling to improve cerebral glucose metabolism and support the molecular processes necessary for memory consolidation and cognitive resilience.
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