Most disease-modifying therapeutic approaches in Alzheimer's disease (AD) aim to 
reduce the accumulation of neurotoxic amyloid-beta (Abeta) peptides as a 
hallmark of AD pathogenesis. Here we report the in vitro basis for a potential 
autologous stem cell-based strategy for widespread delivery of enzymatic 
activities against Abeta formation in the brain. We detected the functional 
induction of two genes upon neuroectodermal conversion of human adult 
mesenchymal stem cells (MSCs), namely F-spondin and neprilysin (CD10), with a 
4,992 + or - 697-fold and 692 + or - 226-fold increase of mRNA levels in 
converted cells compared to MSCs, respectively (n = 3; P < 0.01). These genes 
are known to be involved in the formation and degradation of Abeta peptides, 
respectively. Consistently, coincubation of the neuroectodermally converted MSCs 
with HEK-293 cells stably expressing amyloid precursor protein (APP) lead to a 
significant cell dose-dependent decrease of Abeta peptides. These in vitro 
results indicate that MSCs might be useful vehicles for delivering anti-Abeta 
activity depicting a causal stem cell-based therapeutic approach to treat AD.