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 2016


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

2016 Grants - Rice

Selective Vulnerability of Interneurons in Alzheimer’s Disease

Heather Caroline Rice, Ph.D.
Flanders Interuniversity Institute for Biotechnology (VIB)
Leuven, Belgium

2016 Alzheimer’s Association Research Fellowship (AARF)

What makes certain types of nerve cells more vulnerable to damage during Alzheimer’s disease?

Background
Research suggests that a specific type of nerve cells called interneurons, are selectively vulnerable to damage during Alzheimer’s disease. The loss of a small number of these cells can disrupt the activity of nerve cell networks needed for memory and learning. It is not yet understood why some nerve cells are more vulnerable to damage than others, but it may relate to how they are affected by the build-up of beta-amyloid in the brain. Beta-amyloid is a protein fragment that forms “plaques” in the brain – a hallmark of Alzheimer’s disease.

In initial studies, Heather Rice, Ph.D., and colleagues found that certain interneurons in the hippocampus (a brain region important for memory) have unusually high levels of amyloid precursor protein (APP). APP is the parent protein from which beta-amyloid is produced. Dr. Rice hypothesizes that high levels of APP in interneurons promote increased production of toxic beta amyloid leaving them vulnerable to damage in Alzheimer’s disease.

Research Plan
For their current grant, Dr. Rice and team will study how APP levels relate to the production of beta-amyloid and nerve cell damage in Alzheimer’s-like mice. The researchers will determine the type and location of the interneurons that are the largest contributors to amyloid production. They will also examine the interneurons over time for signs of structural damage and loss of connections to other cells that could lead to impaired function of nerve cell networks.

Impact
The results of this work could provide new information on the molecular mechanisms that lead to nerve cell loss in Alzheimer’s disease. Importantly, this work could help identify novel targets for the development of drug therapies to preserve nerve cell function in Alzheimer’s disease.


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.