Research Area
Aging

Grant Type
Fellowship

Year
2005

Abstract

An important aspect of pathogenesis for Alzheimer’s disease (AD) is the dysfunction of Nerve Growth Factor (NGF) transport in axons, the point of neurotrophic support between neurons. One clue to the pathogenesis of AD comes from studies of Down syndrome (DS), a disorder that is due to trisomy 21 in which AD pathology is present in all patients by the age of 40. We have discovered that overexpression of the gene for the amyloid precursor protein (APP), disrupts the transport of NGF needed to ensure the development and maintenance of neurons for learning and memory. My primary focus is the signaling of NGF. Using the microfluidic neuronal chamber as a platform, I studied the NGF transport pattern in live neuron cells from Down syndrome and normal mice. By generalizing differences on the moving aspects of individual NGF molecules between Down syndrome axons and normal axons, I analyzed the possible mechanisms at molecular level that compromise NGF transport at early onset of neuronal degeneration in DS and AD. The findings in this project sponsored by Hillblom Foundation open up new possibilities for both understanding and treating people with DS and AD which attack the root cause of the disorder so that dementia can be prevented or reversed.