Tau protein hyperphosphorylation and aggregation in Alzheimer's disease and other tauopathies, and possible neuroprotective strategies

Šimić, Goran and Babić Leko, Mirjana and Wray, Selina and Harrington, Charles and Delalle, Ivana and Jovanov-Milošević, Nataša and Bažadona, Danira and Buée, Luc and de Silva, Rohan and Di Giovanni, Giuseppe and Wischik, Claude and Hof, Patrick R. (2016) Tau protein hyperphosphorylation and aggregation in Alzheimer's disease and other tauopathies, and possible neuroprotective strategies. Biomolecules, 6 (1). p. 6. ISSN 2218-273X

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Abnormal deposition of misprocessed and aggregated proteins is a common final pathway of most neurodegenerative diseases, including Alzheimer's disease (AD). AD is characterized by the extraneuronal deposition of the amyloid β (Aβ) protein in the form of plaques and the intraneuronal aggregation of the microtubule-associated protein tau in the form of filaments. Based on the biochemically diverse range of pathological tau proteins, a number of approaches have been proposed to develop new potential therapeutics. Here we discuss some of the most promising ones: inhibition of tau phosphorylation, proteolysis and aggregation, promotion of intra- and extracellular tau clearance, and stabilization of microtubules. We also emphasize the need to achieve a full understanding of the biological roles and post-translational modifications of normal tau, as well as the molecular events responsible for selective neuronal vulnerability to tau pathology and its propagation. It is concluded that answering key questions on the relationship between Aβ and tau pathology should lead to a better understanding of the nature of secondary tauopathies, especially AD, and open new therapeutic targets and strategies.

Item Type: Article
Additional Information: © 2016 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons by Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0).
MeSH: Alzheimer Disease / drug therapy ; Alzheimer Disease / metabolism ; Amyloid beta-Peptides / metabolism ; Animals ; Humans ; Neurofibrillary Tangles ; Neuroprotective Agents / therapeutic use ; Phosphorylation / drug effects ; Protein Processing, Post-Translational / drug effects ; Tauopathies / drug therapy ; Tauopathies / metabolism ; tau Proteins / metabolism
Departments: Hrvatski institut za istraživanje mozga
Katedra za anatomiju i kliničku anatomiju
Katedra za medicinsku biologiju
Depositing User: Marijan Šember
Status: Published
Babić Leko, MirjanaUNSPECIFIED
Harrington, CharlesUNSPECIFIED
Jovanov-Milošević, NatašaUNSPECIFIED
Bažadona, DaniraUNSPECIFIED
de Silva, RohanUNSPECIFIED
Di Giovanni, GiuseppeUNSPECIFIED
Wischik, ClaudeUNSPECIFIED
Date: 6 January 2016
Date Deposited: 08 Mar 2016 12:41
Last Modified: 17 Aug 2020 07:15
Subjects: /
Related URLs:
URI: http://medlib.mef.hr/id/eprint/2537

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