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Oncogenes on my mind: ERK and MTOR signaling in cognitive diseases

Lianne C Krab1, Susanna M I Goorden, Ype Elgersma

  • 1Department of Neuroscience, Erasmus University Medical Center, 3000 CA, Rotterdam, The Netherlands.

Trends in Genetics : TIG
|September 9, 2008
PubMed

Insights

Defects in RAS-ERK and PI3K-MTOR pathways cause neurodevelopmental disorders. Cancer drugs show promise in reversing cognitive deficits in mouse models, offering hope for new treatments.

Area of Science:

  • Neuroscience
  • Genetics
  • Oncology

Background:

  • Genetic disorders like neuro-cardio-facial-cutaneous (NCFC) and Hamartoma syndromes are linked to defects in RAS-ERK and PI3K-MTOR signaling pathways.
  • While these pathways are known for their roles in cell proliferation and cancer, their impact on cognitive function is less understood.

Purpose of the Study:

  • To investigate the cognitive impairments associated with mutations in the RAS-ERK and PI3K-MTOR signaling pathways.
  • To explore the underlying mechanisms of these cognitive deficits using insights from recent animal studies.

Main Methods:

  • Review of recent animal studies focusing on RAS-ERK and PI3K-MTOR signaling pathways.
  • Analysis of cognitive function in mouse models of NCFC and Hamartoma syndromes.

Main Results:

  • Mutations in RAS-ERK and PI3K-MTOR pathways are associated with significant cognitive problems.
  • Cancer drugs targeting these pathways have demonstrated the ability to reverse cognitive deficits in preclinical models.

Conclusions:

  • The RAS-ERK and PI3K-MTOR pathways play a crucial role in cognitive function.
  • Targeting these pathways with existing cancer drugs may offer a therapeutic strategy for cognitive impairments in related genetic disorders.
  • These findings support the potential for clinical trials to test cancer drugs for treating cognitive deficits in NCFC and Hamartoma syndromes.

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