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Extracellular Tau Oligomers Produce An Immediate Impairment of LTP and Memory

M Fá1, D Puzzo1,2, R Piacentini3

  • 1Department of Pathology and Cell Biology and Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, 630 W 168th St. New York, NY 10032 USA.

Scientific Reports
|January 21, 2016
PubMed

Insights

Extracellular tau oligomers (oTau) rapidly impair memory and long-term potentiation (LTP) independently of amyloid-beta (oAβ). This suggests oTau as a potential therapeutic target for Alzheimer

Area of Science:

  • Neuroscience
  • Biochemistry
  • Pathology

Background:

  • Soluble oligomeric forms of amyloid-beta peptide (oAβ) and tau proteins are implicated in Alzheimer's disease (AD) pathogenesis.
  • The current hypothesis suggests oAβ initiates tau pathology, leading to memory loss.
  • The independent role of tau pathology in AD progression requires further investigation.

Purpose of the Study:

  • To investigate the direct impact of extracellular tau oligomers (oTau) on memory and synaptic plasticity.
  • To determine if oTau can induce cognitive deficits independent of amyloid-beta (oAβ) presence.
  • To explore the combined effects of oTau and oAβ on cognitive function.

Main Methods:

  • Exposure of biological systems to extracellular recombinant human tau oligomers (oTau) and monomers.
  • Assessment of long-term potentiation (LTP) and memory function.
  • Utilizing oTau extracted from AD human specimens and naturally produced oTau in transgenic mice.

Main Results:

  • Brief exposure to oTau, but not monomers, caused immediate impairment of LTP and memory within 20 minutes.
  • These effects were observed independently of high oAβ levels.
  • Combined sub-toxic doses of oTau and oAβ synergistically impaired LTP and memory.

Conclusions:

  • Extracellular oTau directly induces synaptic and memory deficits, independent of oAβ.
  • oTau plays a significant role in AD-associated memory loss.
  • These findings highlight oTau as a potential therapeutic target for AD and related neurodegenerative diseases.

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