Michael E. Calhoun, Ph.D.
Hertie-Institute for Clinical Brain Research
Tübingen, Germany

2005 Investigator-Initiated Research Grant

Amyloid plaques and neurofibrillary tangles are two key pathological features found in the brains of people with Alzheimer’s disease. However, it has been difficult for researchers to ascertain how these features interact or which feature might be primarily responsible for the learning and memory losses that herald the disease.

Michael E. Calhoun, Ph.D., and colleagues will address this problem by examining how tangles and plaques affect the activation of genes related to learning. They will use genetically altered mice that produce either human tau, the major component of tangles, or human beta-amyloid, the principal ingredient in plaques.

These genetically altered mice have been used before and are known to model some of the pathological features and symptoms of Alzheimer’s disease. Calhoun will subject the animals to various behavior and learning tasks and examine the activity of learning-related genes in neurons in regions of the brains that have plaques or tangles. The findings may help scientists understand the relative effects of tau and beta-amyloid on learning and memory processes in the brain.