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 2017


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

2017 Grants - Masurkar

Lateral Entorhinal Cortex-CA1 Interactions in Alzheimer’s Disease

Arjun Masurkar, M.D., Ph.D.
New York University School of Medicine
New York, New York

2017 Alzheimer’s Association Clinical Fellowship (AACF)

Why are specific brain regions involved in memory vulnerable to the toxic effects of beta-amyloid?

Background
Nerve cells in the brain communicate with each other via tiny specialized structures called synapses which are essential for memory function. One of the earliest brain changes associated with Alzheimer’s disease is the loss of these important synapses. Evidence suggests that when beta-amyloid accumulates in the brain during Alzheimer’s disease it can damage synapses. It is not yet understood why certain types of nerve cells are more vulnerable than others to the toxic effects of the beta-amyloid protein.

Research Plan
Arjun Masurkar, M.D., Ph.D. and colleagues will study how beta-amyloid oligomers inside nerve cells lead to loss of synapses and disruption in nerve cell communication. Oligomers are small, abnormal clumps of beta-amyloid that are thought to be particularly toxic to nerve cells in the early stages of Alzheimer’s disease. The researchers will focus their efforts on synapses between two brain regions important for learning and memory — the lateral entorhinal cortex and hippocampal CA1 region. The researchers will measure changes in synaptic function and the activity of nerve cell pathways between these regions in Alzheimer’s-like mice. They aim to identify the specific nerve cells most vulnerable to the toxic beta-amyloid oligomers.

Impact
These studies could improve our understanding of the earliest effects of beta-amyloid on nerve cell function in Alzheimer’s disease. The results of this work could also identify new avenues for the development of therapies that protect vulnerable nerve cells and help slow or halt the progression of 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.