The Role of Amyloid-Beta and Tau in the Early Pathogenesis of Alzheimer’s Disease

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

doi:10.12659/MSM.933084

02 September 2021 : Review article

The Role of Amyloid-Beta and Tau in the Early Pathogenesis of Alzheimer’s Disease

Xiaomin Yin^123BC, Yanyan Qiu^1DF, Chenhao Zhao^1F, Zheng Zhou^1F, Junze Bao^1F, Wei Qian^123AE*

DOI: 10.12659/MSM.933084

Med Sci Monit 2021; 27:e933084

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Background Oligomeric Aβ and Synaptic Dysfunction Tau and Synaptic Deficits Mitochondria and Synaptic Degeneration Synaptic Proteins and Synaptic Function Other Factors Related to Aβ and Tau in AD Synapse-Based Therapy in Alzheimer’s Disease Conclusions References

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Figure 1 Feedback mechanisms of synaptic Aβ and tau in the progress of Alzheimer’s disease. Soluble oligomeric Aβ is the primary cause of synaptic dysfunction, whereas synaptic tau is the mediator in the progress. They locate in the synapse and work with receptors, synaptic proteins, and mitochondria to cause synaptic dysfunction, and ultimately lead to cognitive deficits. During the pathogenesis of AD, this is the early event, which occurs long before the formation of neurofibrillary tangles and senile plaques.

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The Role of Amyloid-Beta and Tau in the Early Pathogenesis of Alzheimer’s Disease

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