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Metabolic Profiling of Suprachiasmatic Nucleus Reveals Multifaceted Effects in an Alzheimer’s Disease Mouse Model
Metabolic changes in the brain's internal clock system in a mouse model of Alzheimer's disease
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Abstract
Significant metabolic deficits were observed in the superchiasmatic nucleus (SCN) of Tg2576 Alzheimer's disease mice.
- Reductions in glucose, glutamate, , and glutamine indicate impaired GABAergic glucose oxidation and neurotransmitter cycling.
- Low levels of the redox co-factor NADPH and glutathione suggest a state of redox disbalance.
- There is decreased expression of the core clock protein Bmal1, particularly in activated astrocytes.
- A reduction in GABA transporter 1 (GAT1) expression in astrocytes points to decreased GABA recycling.
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Key numbers
significantly reduced in SCN of
Decrease in levels
Comparison of levels in SCN of Tg2576 vs. wild-type mice.
Glucose and glutamate levels significantly decreased in SCN of
Reduction in glucose and glutamate
Metabolic profiling of SCN in Tg2576 vs. wild-type mice.