Plan to Attend First Science Seminar of the School Year Monday, Nov. 24
Posted on 11/12/2014

All Freeport High School students and staff are invited to attend the first science seminar of the 2014-15 school year. The seminar will be held on Monday, Nov. 24, 2014 from 2:30-3:15 p.m. in the high school Distance Learning Center.

The featured speaker will be Dr. Lisa Miller, Associate Division Director for Spectroscopy and Imaging in the Photon Sciences Directorate at Brookhaven National Laboratory. She is also the spokesperson for Beamlines U2B and U10B at the NSLS.

Shining Synchrotron Light on the Cause of Alzheimer's Disease
Lisa M. Miller, PhD

National Synchrotron Light Source
Brookhaven National Laboratory
Upton, NY 11973

Departments of Chemistry and Biomedical Engineering
Stony Brook University
Stony Brook, NY 11794

Alzheimer's disease (AD) is characterized by the misfolding and plaque-like accumulation of a naturally occurring protein in the brain called amyloid beta (Aβ). This process has been associated with the binding of metal ions such as iron (Fe), copper (Cu), and zinc (Zn). It has been suggested that metal imbalance is involved in plaque formation and may lead to toxic chemistry in the brain that kills neurons. However, the exact role of the misfolded proteins and metal ions in the degenerative process is not yet clear and is the focus of the research in my lab. In this talk, I will explain the inner workings of the synchrotron at Brookhaven National Laboratory and discuss how we use synchrotron X-rays and infrared light to image both the misfolded protein structure and metal ion distribution in Alzheimer's brain tissues. I will compare images of human brain tissue, where a large amount of brain cell death occurs, to mouse models of AD, where little neurodegeneration is observed. The results strongly suggest that metal ions in the brain play a role in brain cell death in AD. These findings may be useful in developing early diagnostic imaging tools for the disease and new therapies for slowing or preventing plaque formation and/or neuron death in the future.