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Related Experiment Video

Updated: May 18, 2026

In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein

In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein

Published on: January 2, 2015

Hypoglycemia induces tau hyperphosphorylation.

Chu-Wan Lee¹, Yao-Hsiang Shih, Shih-Ying Wu

¹Institute of Basic Medical Sciences, National Cheng Kung University, Tainan, Taiwan.

Current Alzheimer Research

|October 6, 2012

Summary

This summary is machine-generated.

Cerebral hypoglycemia, or low brain glucose, triggers cellular energy crisis and activates the AMPK-Akt-GSK3 pathway, leading to tau hyperphosphorylation, a hallmark of Alzheimer's disease.

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Area of Science:

Neuroscience
Biochemistry
Cell Biology

Background:

Cerebral hypoglycemia/hypometabolism is linked to Alzheimer's disease (AD) and aids in clinical diagnosis via brain imaging.
The causal role of cerebral hypoglycemia in AD development versus being a response to reduced neuronal activity is not fully understood.

Purpose of the Study:

To investigate the causal relationship between cerebral hypoglycemia and the molecular changes associated with Alzheimer's disease.

Main Methods:

Cultured differentiated N2a neuroblastoma cells in glucose/pyruvate-deficient media (GDM).
Examined the effects of GDM on mitochondrial membrane potential, AMPK activation, tau phosphorylation, and GSK3α/β and Akt activity.
Induced cerebral hypoglycemia in Wistar rats via intracerebroventricular (icv) streptozotocin (STZ) injection.
Assessed pAMPK, tau phosphorylation, GSK3β, and Akt activity in rat brain regions.
Evaluated hippocampus-dependent spatial learning and memory in rats.

Main Results:

GDM treatment in N2a cells reduced mitochondrial membrane potential and activated AMPK.
GDM increased tau phosphorylation (Ser262, Ser396) and active GSK3α/β, while decreasing active Akt.
STZ-icv injection induced an energy crisis in the hippocampus, evidenced by increased pAMPK.
STZ-icv treatment elevated phosphorylated tau and activated GSK3β, but reduced active Akt in the hippocampus.
Hippocampus-dependent spatial learning and memory were impaired in STZ-icv treated rats.

Conclusions:

Hypoglycemia enhances the AMPK-Akt-GSK3 pathway.
This pathway activation leads to tau hyperphosphorylation, suggesting a direct link between hypoglycemia and AD pathology.