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DOPA Decarboxylase Modulates Tau Toxicity.

Rebecca L Kow1, Carl Sikkema2, Jeanna M Wheeler3

  • 1Geriatrics Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle Division, Washington; Division of Medical Genetics, Department of Medicine, University of Washington, Seattle, Washington.

Biological Psychiatry
|July 29, 2017
PubMed
Summary
This summary is machine-generated.

Loss of the DOPA decarboxylase (DDC) gene, bas-1, reduces tau toxicity in a C. elegans model. This finding suggests DDC suppression of tauopathy may involve levodopa and 5-hydroxytryptophan accumulation.

Keywords:
Aromatic amino acid decarboxylaseDOPA decarboxylaseDopamineNeurodegenerationSerotoninTau

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Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Tau protein aggregates are implicated in neurodegenerative diseases.
  • Loss of D2-family dopamine receptors previously showed promise in ameliorating tauopathy.

Purpose of the Study:

  • Investigate the mechanisms by which D2-family dopamine receptor loss alleviates tau toxicity.
  • Screen dopamine-related genes in C. elegans to identify factors influencing tau toxicity.

Main Methods:

  • Conducted a screen of 45 C. elegans mutations in dopamine-related genes.
  • Assessed the impact of mutations on tau transgene-induced behavioral defects.
  • Analyzed tau accumulation, phosphorylation, and neuron loss.

Main Results:

  • Identified DOPA decarboxylase (DDC) gene, bas-1, as a suppressor of tau toxicity.
  • Loss of bas-1 ameliorated behavioral deficits, reduced tau accumulation, and decreased neuron loss.
  • Other dopamine/serotonin synthesis genes did not affect tau toxicity but were necessary for bas-1 suppression.

Conclusions:

  • Loss of C. elegans DDC bas-1 significantly reduces tau-induced toxicity.
  • Suppression of tau toxicity by bas-1 may involve the accumulation of levodopa and 5-hydroxytryptophan.
  • D2-family dopamine receptor loss did not enhance bas-1 mediated suppression of tauopathy.