Internalized antibodies to the Aβ domain of APP reduce neuronal Aβ and protect against synaptic alterations
Research output: Contribution to journal › Article
Immunotherapy against β-amyloid peptide (Aβ) is a leading therapeutic direction for Alzheimer disease (AD). Experimental studies in transgenic mouse models of AD have demonstrated that Aβ immunization reduces Aβ plaque pathology and improves cognitive function. However, the biological mechanisms by which Aβ antibodies reduce amyloid accumulation in the brain remain unclear. We provide evidence that treatment of AD mutant neuroblastoma cells or primary neurons with Aβ antibodies decreases levels of intracellular Aβ. Antibody-mediated reduction in cellular Aβ appears to require that the antibody binds to the extracellular Aβ domain of the amyloid precursor protein (APP) and be internalized. In addition, treatment with Aβ antibodies protects against synaptic alterations that occur in APP mutant neurons.
|Research areas and keywords||
Subject classification (UKÄ) – MANDATORY
|Journal||Journal of Biological Chemistry|
|Publication status||Published - 2007 Jun 29|