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In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
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A Study on PHF-Tau Network Effected by Apolipoprotein E4.

Yuan Li1, Zhijun Yao2, Yongqing Yang1

  • 1School of Management Science and Engineering, Shandong Technology and Business University, Yantai, People's Republic of China.

American Journal of Alzheimer'S Disease and Other Dementias
|December 1, 2020
PubMed
Summary
This summary is machine-generated.

The Apolipoprotein E 4 Allele (APOE 4) significantly alters brain network properties related to Tau protein in individuals with mild cognitive impairment. APOE 4 carriers exhibit less resilient brain networks, suggesting a role in cognitive dysfunction.

Keywords:
APOE 4mild cognitive impairmentnetwork propertiesnetwork resiliencetau PET brain network

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Area of Science:

  • Neuroscience
  • Genetics
  • Biochemistry

Background:

  • Apolipoprotein E 4 Allele (APOE 4) is a key genetic risk factor for Alzheimer's disease (AD) and mild cognitive impairment (MCI).
  • APOE 4 influences the abnormal modification and aggregation of Tau protein into paired helical filaments (PHF-Tau).

Purpose of the Study:

  • To investigate the impact of APOE 4 on the network properties and resilience of PHF-Tau in the brain.
  • To explore the relationship between APOE 4 status and brain network alterations in individuals with cognitive impairment.

Main Methods:

  • Utilized Positron Emission Tomography (PET) imaging to measure PHF-Tau.
  • Analyzed network properties and resilience in 143 subjects, divided into APOE 4 carriers and noncarriers.

Main Results:

  • APOE 4 carriers demonstrated significant differences in overall PHF-Tau network properties compared to noncarriers.
  • Specific brain regions showed altered betweenness centrality in APOE 4 carriers.
  • APOE 4 carriers exhibited reduced resilience to both targeted and random network node failures.

Conclusions:

  • The presence of the APOE 4 allele is associated with abnormalities in the PHF-Tau protein network.
  • These network alterations may contribute to the pathophysiology of cognitive dysfunction observed in MCI patients.