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Novel antibody reveals intracellular APP C-terminal fragments (iAPP) accumulate in Alzheimer

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Area of Science:

  • Neuroscience
  • Neuropathology
  • Molecular Biology

Background:

  • Accumulation of Amyloid Precursor Protein (APP) C-terminal fragments (CTFs) is observed in Alzheimer's disease (AD) brains.
  • Previous studies relied on biochemical techniques, leaving the neuroanatomical distribution of APP-CTF accumulation unknown in human AD.
  • A novel APP antibody was developed to investigate the morphological distribution of APP-CTF accumulation in postmortem human brain tissue.

Purpose of the Study:

  • To generate and characterize a novel antibody targeting the C-terminus of APP.
  • To investigate the neuroanatomical distribution and morphological characteristics of APP-CTF accumulation in human AD brains.
  • To determine if APP-CTF accumulation represents a neuropathological hallmark of AD.

Main Methods:

  • Generated a novel murine antibody (APP1B) against the C-terminus of APP.
  • Validated antibody specificity using primary human cortical cell cultures from Down syndrome (DS) fetuses and a cell line expressing APP-C99.
  • Performed immunohistochemistry on postmortem human brain samples from individuals with AD (sporadic, autosomal dominant, and DS-AD), controls, and other neurodegenerative diseases.

Main Results:

  • The novel APP1B antibody specifically recognized APP-CTFs in cell cultures.
  • Extensive intracellular 'tangle-like' neuronal APP (iAPP) immunoreactivities were observed in AD-vulnerable brain regions across different AD types.
  • iAPP pathology was absent in controls, DS without AD, and other neurodegenerative diseases, and did not colocalize with tau or ubiquitin.

Conclusions:

  • Intracellular APP C-terminal fragment (iAPP) pathology is proposed as a novel neuropathological hallmark of Alzheimer's disease.
  • The topographical distribution and selective neuronal involvement of iAPP pathology suggest a link between APP dyshomeostasis and tau aggregation.
  • This finding provides new insights into the molecular mechanisms underlying AD pathogenesis.