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Metabolic breakdown: Linking insulin resistance and mitochondrial dysfunction to neurodegeneration in Alzheimer’s disease
How Insulin Resistance and Energy Problems in Brain Cells May Be Linked to Alzheimer's Disease
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Abstract
Insulin resistance and mitochondrial dysfunction are critical contributors to cognitive decline associated with metabolic disorders and neurodegenerative diseases.
- Insulin resistance negatively impacts neuronal metabolism and synaptic function, which may lead to increased neurodegeneration in conditions like Alzheimer's disease and Down syndrome.
- Down syndrome, linked to the triplication of the APP gene, serves as a genetic model for studying early-onset Alzheimer's disease and accelerated aging.
- Intranasal insulin has shown potential in improving cognition in individuals with early Alzheimer's disease and type 2 diabetes by addressing brain insulin resistance.
- Insulin-based therapies may risk desensitizing insulin signaling, potentially exacerbating neurodegenerative conditions.
- Glucagonlike peptide 1 receptor agonists may provide neuroprotective effects by improving insulin sensitivity, metabolism, and synaptic plasticity while reducing oxidative stress and neuroinflammation.
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