Vote Now
Research Grants - 2005


Alzheimer's Assocation Research only
All of alz.org
  • Go to Alz.org
  • Research Center
  • AAIC
  • ISTAART
  • Journal
  • Grants
  • TrialMatch
  • Press
  • Donate
  • Contact Us
Home
Science and Progress
Clinical Trials
Funding and Collaboration
You can Help
Stay Current
Video and Resources

Text Size

Small text Medium text Large text

Research Grants 2005


To view an abstract, select an author from the vertical list on the left side.

2005 Grants - Maysinger

Mechanisms of Nonsteroidal Therapies to Reduce the Risk of Alzheimer's Disease in Menopause

Dusica Maysinger, Ph.D.
McGill University
Montreal, Quebec, Canada

2005 Investigator-Initiated Research Grant

Estrogen is known to have certain neuroprotective properties, and studies have suggested that post-menopausal womenóthat is women with low estrogen levelsómay be more likely to develop Alzheimer's than men of the same age. Other evidence suggests that estrogen may inhibit certain Alzheimer-related pathological processes. Nonetheless, estrogen replacement therapy has proven to be controversial and may not function as an effective risk-lowering strategy. A better understanding of estrogen's role in the brain and the impact of age-related estrogen depletion is needed.

Dusica Maysinger, Ph.D., and colleagues are developing a line of mice to study estrogen and Alzheimer's disease. They will crossbreed mice that are genetically altered to show features of Alzheimer's disease with estrogen-deficient mice. They will assess whether these "menopausal" Alzheimer-like mice develop beta-amyloid deposits at a faster rate than "normal" Alzheimer mice. Beta-amyloid is a tiny protein fragment that may be a key toxic factor in Alzheimer's disease.

They will also study brain tissues from the menopausal mice to investigate a potential molecular explanation for the enhanced risk of Alzheimer's in post-menopausal women. Their goal is to determine if the reduction of estrogen results in the improper relocation of proteins that, as observed in previous studies, may set in motion cellular events that induce beta-amyloid production. Finally, they will assess a treatment regimen that may correct or prevent the relocation of proteins.

The outcome of this work may help explain the role of estrogen in protecting cells and suggest nonestrogen therapies that may safely mimic estrogen's neuroprotective activity.