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Tau pathology does not affect experience-driven single-neuron and network-wide Arc/Arg3.1 responses.

Nikita Rudinskiy, Jonathan M Hawkes, Susanne Wegmann

  • 1Alzheimer's Disease Research Laboratory, Department of Neurology, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown 02129, MA, USA. bhyman@partners.org.

Acta Neuropathologica Communications
|June 12, 2014
PubMed
Summary

Intraneuronal neurofibrillary tangles (NFTs) in tauopathy do not impair experience-dependent gene expression. This suggests NFTs may not directly affect neuronal signaling crucial for memory consolidation in Alzheimer's disease research.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Pathology

Background:

  • Intraneuronal neurofibrillary tangles (NFTs) are hallmarks of Alzheimer's disease and other tauopathies.
  • NFTs are linked to cognitive decline, but their direct impact on neuronal function is unclear.

Purpose of the Study:

  • To investigate if advanced tau pathology, specifically NFTs, affects activity-driven gene expression of Arc in neurons.
  • To determine the impact of NFTs on experience-dependent memory consolidation mechanisms.

Main Methods:

  • Utilized a transgenic mouse model of tauopathy.
  • Examined activity-driven expression of the immediate-early gene Arc in visual cortex and hippocampal neurons in vivo and postmortem.
  • Assessed network-wide Arc expression across different brain regions.

Main Results:

  • Neurons with NFTs showed comparable Arc expression to tangle-free neurons in response to visual stimulation.
  • Tau tangles did not alter the probability of experience-dependent Arc response in visual cortex or hippocampal neurons.
  • Network-wide activity-driven Arc expression was unaffected by tau pathology in all brain regions studied.

Conclusions:

  • Intraneuronal NFTs do not appear to disrupt signaling cascades essential for experience-dependent gene expression.
  • These findings suggest NFTs may not directly impair the neuronal plasticity required for long-term memory formation.