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Zeb Kurth-Nelson Entering Class - 2003 E-mail: kurt0073@umn.edu

Undergraduate Institution and Major/Degree:

Major Advisor(s):

Research Description:

The amyloid cascade hypothesis of Alzheimer's disease (AD) states that overproduction of amyloid beta triggers a series of brain changes that eventually leads to synapse loss and cell death. Before these overt pathologies manifest, however, AD patients and transgenic model animals exhibit symptoms of memory loss. We are testing the hypothesis that a particularly mean form of amyloid beta causes the early symptoms of AD.
This pathogenic species is called Abeta*56 and is a dodecamer of the amyloid beta peptide.

In particular, we are asking whether Abeta*56 is an antagonist of NMDA receptors. Other studies have established that amyloid beta oligomers can inhibit long-term potentiation (LTP), which could explain the memory loss that occurs early in the disease course. If we identify the responsible oligomer and its mechanism of action, then new therapies can selectively target this oligomer.

Lab Rotations:

Courses Taken Beyond the Core Courses:

Conferences Attended:

Committee Members:

• Bob Miller (chair)
• Karen Ashe
• Mark Thomas
• Jan Dubinsky
• Eric Newman (advisor)

Selected Publications and Presentations:

• Redish AD, Kurth-Nelson Z (in press) "Neural models of temporal discounting" in Impulsivity: Theory, Science, and Neuroscience of Discounting G. Madden, W. Bickel, T. Critchfield (eds). APA books.
  
• Redish AD, Jensen S, Johnson A, Kurth-Nelson Z (2007) Reconciling reinforcement learning models with behavioral extinction and renewal:
  implications for addiction, relapse, and problem gambling. Psychological Review 114:784.

• Kurth-Nelson ZL, Redish AD (2004) Micro-Agents: Action-Selection In Temporally Dependent Phenomena Using Temporal Difference Learning Over A Collective Belief Structure. Society for Neuroscience Meeting 2004.