Caenorhabditis elegans as a model organism to study APP function.
The brains of Alzheimer's disease patients show an increased number of senile plaques compared with normal patients. The major component of the plaques is the β-amyloid peptide, a cleavage product of the amyloid precursor protein (APP). Although the processing of APP has been well-described, the physiological functions of APP and its cleavage products remain unclear. This article reviews the multifunctional roles of an APP orthologue, the C. elegans APL-1. Understanding the function of APL-1 may provide insights into the functions and signaling pathways of human APP. In addition, the physiological effects of introducing human β-amyloid peptide into C. elegans are also reviewed. The C. elegans system provides a powerful genetic model to identify genes regulating the molecular mechanisms underlying intracellular β-amyloid peptide accumulation.
Graduate Center, City University of New York, New York, NY, USA.
Collin Y
CY
Ewald
Chris
C
Li
D016564:Amyloid beta-Protein Precursor / Q000502:physiology*; D000818:Animals; D017173:Caenorhabditis elegans / Q000502:physiology*; D029742:Caenorhabditis elegans Proteins / Q000502:physiology*; D002470:Cell Survival / Q000502:physiology; D004195:Disease Models, Animal; D006801:Humans; D008565:Membrane Proteins / Q000502:physiology; D009474:Neurons / Q000502:physiology; D011485:Protein Binding / Q000502:physiology
C084891:APL-1 protein, C elegans; D016564:Amyloid beta-Protein Precursor; D029742:Caenorhabditis elegans Proteins; D008565:Membrane Proteins