The Mayford Laboratory

Research

We study the basic cellular and molecular mechanisms by which we learn (cognitive disorders) and understanding how cells in the againg brain die (neurodegenerative disease and aging).

Neurons in the mouse amygdala are stained using antibodies against β-galactosidase (red) and GFP (green). GFP is driven by the fos promoter, which also drives tTA. β-galactosidase is driven by a tet-O promoter, which also drives tTA. Fos promoter activition leads to permanent tagging of neurons.

Cognitive Disorders
Mental retardation affects approximately one percent of school-age children, yet a specific cause is identifiable less than half the time. Many of these cases likely result from an underlying developmental or genetic abnormality. The general approach is as follows:

• Identify learning and memory disorders as part of a large-scale genetic screen.
• Use current advances in genomic technology to rapidly identify the mutant gene.
• Identify underlying mechanisms of gene function by studying the brain and behavior.
• Identify homologous mutations and mechanisms in human cognitive disorders.

Neurodegenerative Disease and Aging
During normal metabolic activity the cells in our body generate toxic byproducts known as free radicals. These toxic molecules are thought to contribute both to the normal cellular decline with age and to the death of neurons in a number of pathological conditions such as Alzheimer's disease, Parkinson's disease, and stroke. The general approach is as follows:

• Identify cells resistant to free radical damage.
• Use current advances in genomic technology to rapidly identify the mutant gene.
• Determine whether the mutation slows the aging or neural degeneration process.
• Identify the homologous genes and mutations in humans to determine whether similar mechanisms apply.