James Andy Snipes

Tau pathology reprograms glucose metabolism to support glutamatergic activity and excitatory imbalance

This study investigates how tau pathology affects metabolism and excitatory activity in mouse models, finding that it preserves glucose tolerance and shifts metabolic flux toward glutamate synthesis.

High-Resolution Spatial Profiling of Microglia Reveals Proximity Associated Immunometabolic Reprogramming in Alzheimers Disease

This study uses spatial transcriptomics to show that proximity to amyloid plaques in AD models alters microglial metabolism, revealing conserved patterns in human tissue.

Kir6.2-KATP channels alter glycolytic flux to modulate cortical activity, arousal, and sleep-wake homeostasis

This study shows that Kir6.2-KATP channels regulate glycolytic flux, neuronal activity, and sleep-wake transitions by modulating lactate dynamics and metabolic stability.

Novel method for collecting hippocampal interstitial fluid extracellular vesicles (EV-ISF) reveals sex-dependent changes in microglial EV proteome in response to Aβ pathology

The paper develops a method to collect hippocampal interstitial fluid extracellular vesicles (EVISF) and finds sex-dependent changes in microglial EV proteome related to Aβ pathology.

Ethanol exposure alters Alzheimer's-related pathology, behavior, and metabolism in APP/PS1 mice

This study shows chronic ethanol exposure worsens Alzheimer's-like pathology, behavior, and metabolism in APP/PS1 mice by increasing amyloid plaques, altering brain metabolism, and affecting behavior.

Acute hyper- and hypoglycemia uncouples the metabolic cooperation between glucose and lactate to disrupt sleep

This study shows that acute hyper- and hypoglycemia disrupt the metabolic cooperation between glucose and lactate in the brain, affecting sleep-wake cycles.

Kir6.2-containing KATP channels are necessary for glucose dependent increases in amyloid-beta and Alzheimer's-related pathology

This study shows that Kir6.2-KATP channels are necessary for hyperglycemia-induced increases in amyloid-beta and Alzheimer's pathology by regulating lactate transport and Aβ release.

Sulfonylureas target the neurovascular response to decrease Alzheimer's pathology

This study shows that sulfonylureas reduce Alzheimer's pathology by targeting vascular KATP channels, decreasing amyloid-beta aggregation and improving vascular function in mice.