Abstract:
:The senile plaques (SPs) and neurofibrillary tangles (NFTs) are the two major pathological hallmarks of AD, which are composed of β-amyloid protein and Tau protein. So the β-amyloid protein (Aβ) and Tau oligomers (oTau) are the majority in the pathology of AD. Recently, the spreading of Aβ and oTau in the brain of AD patients has received heated value. In this review, we summarize recent research progress and aim to figure out the spreading mechanism of Aβ and Tau in AD via introduction of the formation, release, uptake, diffusion between different brain regions, and the propagation principle of Aβ and Tau. Although the mechanisms of the spreading pathology in AD are still not very clear, increasing discoveries confirm that Aβ and oTau could transmit from one neuron to another along the anatomical connected synapses. Meanwhile, a mass of studies also report that they have a totally opposite hierarchical spatiotemporal pattern of spreading in cerebral areas. In addition, Tau proteins might mediate Aβ toxicity in the brain, and they might have synergistic roles with each other. So some therapies have emerged, such as inhibiting the release, preventing the oligomerization, and blocking the uptake. This review would be helpful to comprehend the mechanism of transmission in AD and provide a new way to the targeted therapy.
journal_name
Neurotox Resjournal_title
Neurotoxicity researchauthors
Lv ZY,Tan CC,Yu JT,Tan Ldoi
10.1007/s12640-017-9765-2subject
Has Abstractpub_date
2017-11-01 00:00:00pages
707-722issue
4eissn
1029-8428issn
1476-3524pii
10.1007/s12640-017-9765-2journal_volume
32pub_type
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