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TTC7 and Hyccin Regulate Neuronal Aβ42 Accumulation and its Associated Neural Deficits in Aβ42-Expressing Drosophila

Minghao Sun1, Yinghui Zhao1,2, Men Han3

  • 1Shanghai Advanced Research Institute, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.

Journal of Alzheimer'S Disease : JAD
|August 15, 2018
PubMed

Insights

Downregulating TTC7 and Hyccin proteins reduces amyloid-β accumulation in Alzheimer's disease models. This finding supports the RBO/Efr3-PI4KIIIα complex as a potential therapeutic target for AD.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Neuronal amyloid-β (Aβ) accumulation is central to Alzheimer's disease (AD) pathogenesis.
  • Lipids on the plasma membrane influence Aβ conformation and toxicity.
  • Previous studies linked Rolling Blackout (RBO) or phosphatidylinositol-4-kinase type IIIα (PI4KIIIα) downregulation to reduced Aβ accumulation in a Drosophila AD model.

Purpose of the Study:

  • To investigate the role of TTC7 and Hyccin (FAM126A) in neuronal Aβ accumulation and AD-related deficits.
  • To determine if TTC7 and Hyccin homologs function similarly to RBO/PI4KIIIα in regulating Aβ.

Main Methods:

  • Genetic downregulation and overexpression of TTC7 and Hyccin in a Drosophila model expressing Aβ42.
  • Assessment of neuronal Aβ accumulation, synaptic function, motor deficits, and survival rates.

Main Results:

  • Genetic downregulation of Drosophila TTC7 and Hyccin significantly reduced neuronal Aβ accumulation.
  • TTC7 and Hyccin downregulation also ameliorated synaptic and motor defects and prolonged survival in Aβ42 flies.
  • Overexpression of TTC7 and Hyccin exacerbated Aβ accumulation and associated deficits.

Conclusions:

  • The RBO/TTC7/PI4KIIIα/Hyccin complex regulates neuronal Aβ accumulation and associated neural deficits in Drosophila.
  • These findings reinforce the potential of targeting the RBO/Efr3-PI4KIIIα complex therapeutically for Alzheimer's disease.
Keywords:
Alzheimer’s diseaseDrosophilaHyccinPI4KIIIαTTC7amyloid-β

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