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2008-A-021-FEL - Abstract

Grant Information

Grant
2008-A-021-FEL
Aging - Fellowship
Title
Cholinergic terminal structure and function in Down syndrome
Investigator
Rachel Nosheny, PhD
Institution
Stanford University
Neuroscience Institute
Funding Status
  • Completed
  • 3 years, $60,000 per year
  • 7/1/2008 to 6/30/2011

Abstract

2008-A-021-FEL - Abstract
Brief Summary
"Cholinergic Terminal Structure and Function in Down Syndrome"

The objective of my research is to understand mechanisms of neurodegeneration that cause cognitive decline in Down syndrome (DS) and Alzheimer’s disease (AD). The long-term goal is to identify molecular targets that can be used to design drugs and other therapies to improve cognition in those affected by these disorders.

In DS, an extra copy of the genes on chromosome 21 leads to a variety of physical and mental symptoms. Individuals with DS often experience delayed physical and language development and mental retardation. In addition, they universally exhibit the changes in brain structure and function associated with AD by age 40, and most individuals with DS eventually show learning and memory deficits similar to those seen in AD. Ts65Dn mice, which contain an extra copy of 140 mouse genes homologous to those on human chromosome 21, model DS. They exhibit learning and memory deficits, age-related loss of basal forebrain cholinergic neurons, and disruption of retrograde transport of target-derived neurotrophic factors necessary for the survival of these neurons. We have recently discovered that neurotrophic factor-mediated signaling pathways are up-regulated in Ts65Dn mice, whereas the expression of key cholinergic receptors is decreased.

We are currently identifying specific brain areas and specific regions within brain cells that show abnormal expression of neuroprotective factors and neurotransmitter receptors to understand the consequences of these changes for brain function. In addition, we are exploring the mechanism responsible for these changes by studying the contributions of specific genes triplicated in Ts65Dn mice and other DS mouse models.

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