The Accumulation of Tau in Postsynaptic Structures: A Common Feature in Multiple Neurodegenerative Diseases?

Peter J. Teravskis, Karen H. Ashe, Dezhi Liao

Research output: Contribution to journalReview articlepeer-review

17 Scopus citations


Increasingly, research suggests that neurodegenerative diseases and dementias are caused not by unique, solitary cellular mechanisms, but by multiple contributory mechanisms manifesting as heterogeneous clinical presentations. However, diverse neurodegenerative diseases also share common pathological hallmarks and cellular mechanisms. One such mechanism involves the redistribution of the microtubule associated protein tau from the axon into the somatodendritic compartment of neurons, followed by the mislocalization of tau into dendritic spines, resulting in postsynaptic functional deficits. Here we review various signaling pathways that trigger the redistribution of tau to the cell body and dendritic tree, and its mislocalization to dendritic spines. The convergence of multiple pathways in different disease models onto this final common pathway suggests that it may be an attractive pathway to target for developing new treatments for neurodegenerative diseases.

Original languageEnglish (US)
Pages (from-to)503-520
Number of pages18
Issue number5-6
StatePublished - Oct 1 2020

Bibliographical note

Funding Information:
The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: NIH Grant Numbers R61 NS115089-01 (DL); R21-NS084007-01 (DL); R21-NS096437-01 (DL); R01-NS79374 (KHA); R01-AG60766 (KHA); Michael J. Fox Foundation Grant (DL); UMN-Mayo Partnership Grant (DL); Minnesota Higher Education Grant (DL).

Publisher Copyright:
© The Author(s) 2020.


  • AMPA receptors
  • Alzheimer’s disease
  • FTDP-17
  • Huntington’s disease
  • MAPT
  • Parkinson’s disease
  • dendritic spines
  • neuronal polarity
  • synaptic plasticity
  • tau


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