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Synaptic tau: A pathological or physiological phenomenon?

Published version
Peer-reviewed

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Authors

Robbins, Miranda 
Clayton, Emma 
Kaminski Schierle, Gabriele S.  ORCID logo  https://orcid.org/0000-0002-1843-2202

Abstract

Abstract: In this review, we discuss the synaptic aspects of Tau pathology occurring during Alzheimer’s disease (AD) and how this may relate to memory impairment, a major hallmark of AD. Whilst the clinical diagnosis of AD patients is a loss of working memory and long-term declarative memory, the histological diagnosis is the presence of neurofibrillary tangles of hyperphosphorylated Tau and Amyloid-beta plaques. Tau pathology spreads through synaptically connected neurons to impair synaptic function preceding the formation of neurofibrillary tangles, synaptic loss, axonal retraction and cell death. Alongside synaptic pathology, recent data suggest that Tau has physiological roles in the pre- or post- synaptic compartments. Thus, we have seen a shift in the research focus from Tau as a microtubule-stabilising protein in axons, to Tau as a synaptic protein with roles in accelerating spine formation, dendritic elongation, and in synaptic plasticity coordinating memory pathways. We collate here the myriad of emerging interactions and physiological roles of synaptic Tau, and discuss the current evidence that synaptic Tau contributes to pathology in AD.

Description

Funder: infinitus china ltd.

Keywords

Review, Plasticity, Tau, Synapses, Memory, Alzheimer’s disease, Neurodegeneration

Journal Title

Acta Neuropathologica Communications

Conference Name

Journal ISSN

2051-5960

Volume Title

9

Publisher

BioMed Central
Sponsorship
wellcome trust (065807/Z/01/Z, 203249/Z/16/Z)
medical research council (MR/K02292X/1)
michael j. fox foundation for parkinson's research (16238)
alzheimer’s research uk (ARUK-PG013-14)
engineering and physical sciences research council (EP/L015889/1)