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 2015


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

2015 Grants - Llorens-Martín

GSK-3ß and Adult Neurogenesis: Therapeutic Potential for Alzheimer's Disease

María Llorens-Martín, Ph.D.
Center for Networked Biomedical Research on Neurodegenerative Diseases
Madrid, Spain

2015 New Investigator Research Grant

Does GSK-3 beta protein contribute to the development of Alzheimer’s disease by preventing the generation of new nerve cells in the brain?

Background
Recent studies have shown that certain brain regions produce new nerve cells throughout life in a process called neurogenesis. This constant regeneration likely helps protect the brain from neurodegenerative diseases such as Alzheimer’s, which involve the progressive loss of nerve cells. One brain region, the hippocampus, experiences more nerve cell regeneration than other regions. The hippocampus is vital for learning and memory and is affected early in Alzheimer’s disease. Recent research has shown that a protein called glycogen synthase kinase-3 beta (GSK-3 beta) becomes abnormally activated in Alzheimer’s disease. Such activation may inhibit the development and survival of new nerve cells in the hippocampus and other parts of the brain. However, scientists are unsure exactly how GSK-3 beta exerts its toxicity.

Research Plan
In initial studies with mice, María Llorens-Martín, Ph.D., and colleagues have found abnormal GSK-3 beta activity can damage hippocampal nerve cells in several ways. For example, it can promote inflammation in the brain that leads to nerve cell degeneration and death. However, GSK-3 beta may also affect nerve cell health more directly, in ways that do not involve brain inflammation.

For this grant, Dr. Llorens-Martín and colleagues plan to identify ways that GSK-3 beta directly promotes damage in the hippocampus. First, they will develop a novel mouse model that has high levels of GSK-3 beta but does not develop brain inflammation. This will allow them to study the effects of GSK-3 beta independently from brain inflammation. The team will then assess how GSK-3 beta activity affects the production of new hippocampal nerve cells and brain function in these mice.

Impact
The results of this study may shed new light on the involvement of GSK-3 beta in the earliest stages of Alzheimer’s disease. Additionally, these studies could help lead to the future development of nerve cell regeneration therapies for preventing or slowing Alzheimer’s disease progression.


Alzheimer's Association International Conference | July 16-20, 2017, London, England

Abstract Submissions Now Open

The Scientific Program Committee is now accepting submissions for poster
presentations, oral presentations and featured research sessions.