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Related Experiment Video

Updated: Nov 18, 2025

Author Spotlight: Understanding the Impact of Pathological Proteins on Axonal Transport in Neurodegenerative Diseases

Author Spotlight: Understanding the Impact of Pathological Proteins on Axonal Transport in Neurodegenerative Diseases

Published on: December 22, 2023

Isoform-selective decrease of glycogen synthase kinase-3-beta (GSK-3β) reduces synaptic tau phosphorylation,

Ana Claudia Amaral^1,2, Beatriz G Perez-Nievas^1,2, Michael Siao Tick Chong^1,2

¹Neurology Department, Massachusetts General Hospital, Boston, MA, USA.

|February 8, 2021

Summary

This summary is machine-generated.

Reducing glycogen synthase kinase-3-beta (GSK-3β) levels lessens pathological tau changes in Alzheimer disease models. This suggests GSK-3β is a promising therapeutic target for tauopathies.

Keywords:

Biological Sciences Cellular Neuroscience Neuroscience

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Area of Science:

Neuroscience
Biochemistry
Pharmacology

Background:

Aberrant glycogen synthase kinase-3-beta (GSK-3β) activation is linked to tau hyperphosphorylation and aggregation in Alzheimer disease (AD).
This pathological cascade contributes to neuronal damage and cognitive decline in AD and other tauopathies.

Purpose of the Study:

To investigate if partial reduction of GSK-3β activity can mitigate pathological tau changes.
To assess the impact of reduced GSK-3β on tau hyperphosphorylation, aggregation, and spreading in vivo and in vitro.

Main Methods:

Adeno-associated viruses (AAVs) were used to express human wild-type tau (hTau) in the entorhinal cortex of wild-type and GSK-3β hemi-knockout (GSK-3β-HK) mice.
Tau pathology, including hyperphosphorylation and spreading, was analyzed in GSK-3β-HK mice.
Aggregation of exogenous FTD-mutant tau was assessed in primary neuronal cultures from GSK-3β-HK mice.

Main Results:

GSK-3β-HK mice exhibited significantly reduced accumulation of hyperphosphorylated tau in synapses.
A significant decrease in tau protein spread between neurons was observed in GSK-3β-HK mice.
Primary neuronal cultures from GSK-3β-HK mice showed significantly reduced aggregation of exogenous FTD-mutant tau.

Conclusions:

Partial reduction of GSK-3β activity effectively suppresses tau-initiated neurodegenerative changes.
Targeting GSK-3β represents a promising therapeutic strategy for Alzheimer disease and other tauopathies.