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Translational Neuroscience

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Tau-mediated synaptic damage in Alzheimer’s disease

Santosh Jadhav
  • Institute of Neuroimmunology, Slovak Academy of Sciences, Centre of Excellence for Alzheimer’s Disease and Related Disorders, Dubravska 9, 845 10 Bratislava, Slovak Republic
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Veronika Cubinkova
  • Institute of Neuroimmunology, Slovak Academy of Sciences, Centre of Excellence for Alzheimer’s Disease and Related Disorders, Dubravska 9, 845 10 Bratislava, Slovak Republic
  • Axon Neuroscience SE, Grosslingova 45, Bratislava, Slovak Republic
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Ivana Zimova
  • Institute of Neuroimmunology, Slovak Academy of Sciences, Centre of Excellence for Alzheimer’s Disease and Related Disorders, Dubravska 9, 845 10 Bratislava, Slovak Republic
  • Axon Neuroscience SE, Grosslingova 45, Bratislava, Slovak Republic
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Veronika Brezovakova
  • Institute of Neuroimmunology, Slovak Academy of Sciences, Centre of Excellence for Alzheimer’s Disease and Related Disorders, Dubravska 9, 845 10 Bratislava, Slovak Republic
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Aladar Madari
  • Small animal clinic, University of Veterinary Medicine and Pharmacy, Komenskeho 73, Kosice, Slovak Republic
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Viera Cigankova
  • Department of Anatomy, Histology and Physiology, University of Veterinary Medicine and Pharmacy, Komenskeho 73, 041 81 Kosice, Slovak Republic
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Norbert Zilka
  • Institute of Neuroimmunology, Slovak Academy of Sciences, Centre of Excellence for Alzheimer’s Disease and Related Disorders, Dubravska 9, 845 10 Bratislava, Slovak Republic
  • Axon Neuroscience SE, Grosslingova 45, Bratislava, Slovak Republic
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
Published Online: 2015-10-23 | DOI: https://doi.org/10.1515/tnsci-2015-0023

Abstract

Synapses are the principal sites for chemical communication between neurons and are essential for performing the dynamic functions of the brain. In Alzheimer’s disease and related tauopathies, synapses are exposed to disease modified protein tau, which may cause the loss of synaptic contacts that culminate in dementia. In recent decades, structural, transcriptomic and proteomic studies suggest that Alzheimer’s disease represents a synaptic disorder. Tau neurofibrillary pathology and synaptic loss correlate well with cognitive impairment in these disorders. Moreover, regional distribution and the load of neurofibrillary lesions parallel the distribution of the synaptic loss. Several transgenic models of tauopathy expressing various forms of tau protein exhibit structural synaptic deficits. The pathological tau proteins cause the dysregulation of synaptic proteome and lead to the functional abnormalities of synaptic transmission. A large body of evidence suggests that tau protein plays a key role in the synaptic impairment of human tauopathies.

Keywords: Alzheimer’s disease; Synaptic loss; Tau protein; Neurofibrillary degeneration; Tauopathies; Tau mislocalization; Transgenic models

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About the article

Received: 2015-07-31

Accepted: 2015-10-04

Published Online: 2015-10-23


Citation Information: Translational Neuroscience, ISSN (Online) 2081-6936, DOI: https://doi.org/10.1515/tnsci-2015-0023.

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©2015 Santosh Jadhav et al.. This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License. BY-NC-ND 3.0

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