Metabolic Influences on Cognitive Function and Alzheimer's Disease
Summary
Metabolic health profoundly shapes brain ageing and influences the risk and progression of Alzheimer’s disease. Dysregulation of glucose and lipid metabolism, as seen in insulin resistance, type 2 diabetes and obesity, exacerbates neuroinflammatory and vascular processes that impair synaptic function and promote neurodegeneration. Energy deficits arising from mitochondrial dysfunction and oxidative stress compromise neuronal resilience, while chronic hyperglycaemia and dyslipidaemia accelerate amyloid-β deposition and tau hyperphosphorylation. Conversely, lifestyle and pharmacological interventions targeting metabolic pathways have shown promise in preserving cognitive performance and attenuating hallmark Alzheimer’s pathologies. Understanding these metabolic–neurodegenerative links is crucial for developing preventative and therapeutic strategies with global relevance.
Research from Nature Portfolio
Recent investigations have demonstrated that higher insulin resistance, measured by the homeostasis model assessment (HOMA-IR), correlates with poorer performance in verbal memory and executive tasks among cognitively normal adults, alongside increased cerebrospinal fluid tau but unchanged amyloid-β levels. In a longitudinal cohort of older individuals, escalating insulin resistance over six years was associated with a measurable decline in global cognitive scores, underscoring its role as a dynamic and modifiable risk factor for age-related cognitive impairment.
Metabolic Influences on Cognitive Function and Alzheimer's Disease publication trend
The graph below shows the total number of articles in metabolic influences on cognitive function and alzheimer's disease across all publications each year (not limited to Nature Index journals).
Technical terms
Homeostasis Model Assessment of Insulin Resistance (HOMA-IR): An index derived from fasting blood glucose and insulin levels to estimate peripheral insulin sensitivity.
Triglyceride-glucose index (TyG): A surrogate marker of insulin resistance calculated from fasting triglyceride and glucose concentrations.
Amyloid-β (Aβ): Peptide fragments that aggregate into extracellular plaques, a core neuropathological feature of Alzheimer’s disease.
Tau protein: A neuronal microtubule-associated protein that, when abnormally phosphorylated, forms intracellular neurofibrillary tangles in Alzheimer’s disease.
References
- Insulin resistance is associated with reductions in specific cognitive domains and increases in CSF tau in cognitively normal adults. Scientific Reports (2017).
- Insulin Resistance is Associated with Cognitive Decline Among Older Koreans with Normal Baseline Cognitive Function: A Prospective Community-Based Cohort Study. Scientific Reports (2018).
- The association of glucose metabolism measures and diabetes status with Alzheimer’s disease biomarkers of amyloid and tau: A systematic review and meta-analysis. Neuroscience & Biobehavioral Reviews (2024).
- The relationship of insulin resistance and diabetes to tau PET SUVR in middle-aged to older adults. Alzheimer's Research & Therapy (2023).
- Alzheimer Disease Pathology and Neurodegeneration in Midlife Obesity: A Pilot Study. Aging and Disease (2024).
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