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Trends Cell Biol. 2015 Jan;25(1):46-53. doi: 10.1016/j.tcb.2014.07.005. Epub 2014 Aug 26.

Connecting the dots between tau dysfunction and neurodegeneration.

Author information

1
Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
2
Clem Jones Centre for Ageing Dementia Research, Queensland Brain Institute, The University of Queensland, Brisbane, QLD 4072, Australia.
3
Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Electronic address: mel_feany@hms.harvard.edu.

Abstract

Tauopathies are devastating and ultimately fatal neurodegenerative diseases, which are histopathologically defined by insoluble filamentous deposits of abnormally phosphorylated tau protein within neurons and glia. Identifying the causes of abnormal tau phosphorylation and subsequent aggregation has been the focus of much research, and is currently a major target for the development of therapeutic interventions for tauopathies, including Alzheimer's disease (AD). Much has recently been learned about the sequence of events that lead from tau dysfunction to neuronal death. This review focuses on the cascade of events that are catalyzed by pathological tau, and highlights current and potential therapeutic strategies to target this pathway.

KEYWORDS:

Alzheimer; actin; cell cycle; chromatin; tauopathy; therapeutics

PMID:
25172552
PMCID:
PMC4275400
DOI:
10.1016/j.tcb.2014.07.005
[Indexed for MEDLINE]
Free PMC Article

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