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Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
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APP/Aβ structural diversity and Alzheimer's disease pathogenesis.

Alex E Roher1, Tyler A Kokjohn2, Steven G Clarke3

  • 1Division of Neurobiology, Barrow Neurological Institute, Phoenix, AZ 85013, USA; Division of Clinical Education, Midwestern University, Glendale, AZ 85308, USA.

Neurochemistry International
|August 17, 2017
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Summary

Modified amyloid-beta (Aβ) species, resulting from posttranslational modifications, are key drivers of Alzheimer's disease (AD) pathology and dementia progression. Understanding these altered Aβ forms is crucial for developing new AD biomarkers and treatments.

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Pathology

Background:

  • The amyloid cascade hypothesis implicates amyloid-beta (Aβ) in Alzheimer's disease (AD) dementia.
  • Current AD therapies target monomeric and oligomeric Aβ 1-40 and 1-42.
  • Alternative APP processing and posttranslational modifications (PTMs) generate diverse Aβ species.

Purpose of the Study:

  • To propose that amplified production and modification of Aβ species accelerate AD neurodegeneration.
  • To catalog Aβ PTMs, including isoAsp, pyroglutamate, and Met35 oxidation.
  • To investigate how these modifications impact Aβ structure, toxicity, and propagation.

Main Methods:

  • Literature survey to catalog Aβ PTMs.
  • Analysis of the structural and biophysical properties of modified Aβ species.
  • Correlation of modified Aβ species with AD pathology and dementia.

Main Results:

  • Identified Aβ PTMs, such as isoAsp, pyroglutamate, and Met35 oxidation, are prevalent in AD.
  • These modifications alter Aβ structure, increasing toxicity, aggregation, and resistance to degradation.
  • Modified Aβ species exhibit prion-like seeding and propagation, contributing to neurodegeneration.

Conclusions:

  • Accumulation of modified Aβ species is intrinsically linked to dementia progression in AD.
  • Specific Aβ conformations and PTMs drive neurotoxicity and brain-wide amyloid transmission.
  • Systematic examination of Aβ PTMs can yield essential biomarkers for AD staging and therapeutic development.