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Pathogenic Feed-Forward Mechanisms in Alzheimer's and Parkinson's Disease Converge on GSK-3

Abdalla M Albeely1, Scott D Ryan1, Melissa L Perreault1

  • 1Department of Molecular and Cellular Biology, University of Guelph, Guelph, ON, Canada.

Brain Plasticity (Amsterdam, Netherlands)
|January 2, 2019
PubMed

Insights

Alzheimer's and Parkinson's diseases share common pathways involving glycogen synthase kinase-3 (GSK-3). Targeting GSK-3 and related pathways may offer new combination therapies for these neurodegenerative diseases.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Pathology

Background:

  • Alzheimer's disease (AD) and Parkinson's disease (PD) exhibit shared pathological hallmarks.
  • Common signaling deficits include altered cholinergic, neurotrophin, and insulin signaling.
  • Cell stress cascades lead to proteinopathy, mitochondrial dysfunction, and neuronal death in both AD and PD.

Purpose of the Study:

  • To provide a unified overview of glycogen synthase kinase-3 (GSK-3) involvement in AD and PD.
  • To elucidate the mechanisms linking shared pathological processes in AD and PD.
  • To identify feed-forward pathways contributing to disease progression.

Main Methods:

  • Literature review and synthesis of existing research on GSK-3 in neurodegenerative diseases.
  • Analysis of signaling pathways and cellular stress cascades.
  • Identification of interconnected neuropathological mechanisms.

Main Results:

  • GSK-3 is central to intertwined feed-forward loops exacerbating AD and PD.
  • GSK-3 regulates multiple biological processes contributing to neuropathology.
  • Shared pathways highlight common therapeutic targets.

Conclusions:

  • GSK-3 plays a pivotal role in the convergence of AD and PD pathologies.
  • Understanding these interconnected pathways is crucial for therapeutic development.
  • Combination therapies targeting multiple facets of AD/PD neuropathology are a necessary next step.
Keywords:
Alzheimer’s diseaseGSK-3Parkinson’s diseasecombination therapyfeed-forward mechanisms

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