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Updated: Mar 2, 2026

Real-Time Impedance-based Cell Analyzer as a Tool to Delineate Molecular Pathways Involved in Neurotoxicity and Neuroprotection in a Neuronal Cell Line
08:23

Real-Time Impedance-based Cell Analyzer as a Tool to Delineate Molecular Pathways Involved in Neurotoxicity and Neuroprotection in a Neuronal Cell Line

Published on: August 9, 2014

11.8K

Tau at the Crossroads between Neurotoxicity and Neuroprotection

Sarah L DeVos1, Bradley T Hyman1

  • 1Massachusetts General Hospital, Harvard Medical School, Department of Neurology, MassGeneral Institute for Neurodegenerative Disease, Charlestown, MA 02129, USA.

Neuron
|May 19, 2017
PubMed

Insights

Specific tau phosphorylation, contrary to prior belief, is neuroprotective. This finding, which mimics tau ablation, reveals the intricate role of tau biology in both neuroprotection and neurotoxicity.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Tau phosphorylation has been traditionally viewed as a toxic event in neurodegenerative diseases.
  • Recent research suggests a more complex role for tau phosphorylation, potentially involving protective mechanisms.

Purpose of the Study:

  • To investigate the neuroprotective potential of specific tau phosphorylation events.
  • To contrast the established neurotoxic hypothesis with emerging neuroprotective findings regarding tau.

Main Methods:

  • Utilized genetic and biochemical approaches to study tau phosphorylation.
  • Compared the effects of specific tau phosphorylation with the consequences of tau ablation in cellular and/or animal models.

Main Results:

  • Demonstrated that certain tau phosphorylation sites confer neuroprotection.
  • Observed that this specific phosphorylation phenocopies the effects of complete tau ablation, suggesting a shared protective pathway.

Conclusions:

  • Challenges the long-held view of tau phosphorylation as solely detrimental.
  • Highlights the dual role of tau biology, encompassing both neurotoxic and neuroprotective functions, dependent on specific phosphorylation states.
Keywords:
Alzheimer’s diseaseamyloid-betaantisense oligonucleotidekinaseknockdownneuroprotectivep38 gammaphosphorylationtau

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