Dendritic/Post-synaptic Tau and Early Pathology of Alzheimer's Disease

Xiaomin Yin; Chenhao Zhao; Yanyan Qiu; Zheng Zhou; Junze Bao; Wei Qian

doi:10.3389/fnmol.2021.671779

Dendritic/Post-synaptic Tau and Early Pathology of Alzheimer's Disease

Front Mol Neurosci. 2021 Jun 25:14:671779. doi: 10.3389/fnmol.2021.671779. eCollection 2021.

Authors

Xiaomin Yin^{1

2

3}, Chenhao Zhao¹, Yanyan Qiu¹, Zheng Zhou¹, Junze Bao¹, Wei Qian^{1

2

3}

Affiliations

¹ Department of Biochemistry and Molecular Biology, Medical School, Nantong University, Nantong, China.
² Jiangsu Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education of China, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, China.
³ NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Nantong University, Nantong, China.

Abstract

Microtubule-associated protein tau forms insoluble neurofibrillary tangles (NFTs), which is one of the major histopathological hallmarks of Alzheimer's disease (AD). Many studies have demonstrated that tau causes early functional deficits prior to the formation of neurofibrillary aggregates. The redistribution of tau from axons to the somatodendritic compartment of neurons and dendritic spines causes synaptic impairment, and then leads to the loss of synaptic contacts that correlates better with cognitive deficits than amyloid-β (Aβ) aggregates do in AD patients. In this review, we discuss the underlying mechanisms by which tau is mislocalized to dendritic spines and contributes to synaptic dysfunction in AD. We also discuss the synergistic effects of tau and oligomeric forms of Aβ on promoting synaptic dysfunction in AD.

Keywords: Alzheimer’s disease; cognitive impairment; post-synapse; synaptic localization; tau.

Publication types

Review