Each summer, students are invited to intern in the Penn FTD Center to gain valuable experience in neurodegenerative disease research. Here, we highlight the work of three undergraduate students who interned with Dr. David Irwin this summer. These students analyzed brain tissue samples from our brain bank program to understand the pathology of neurodegenerative diseases including frontotemporal degeneration (FTD) and Alzheimer’s Disease (AD).
Cecilia Zhou, Haverford College (class of 2019)
Researchers studying the pathology of neurodegenerative disease need to apply colored stains to brain tissue samples to identify pathologic proteins in brain cells. This often involves the same tissue sample being stained and analyzed multiple times. This summer, Cecilia studied how reliable the measurement of proteins was between multiple staining analyses of the same tissue sample. She studied brain tissue samples from 100 FTD patients (80 behavioral variant FTD, 20 primary progressive aphasia) patients, and each brain tissue sample was stained and analyzed twice for the same protein. Cecilia found that the quantity of proteins identified from the 2nd analysis differed slightly from the quantity of proteins identified from the 1st analysis, but that a statistical method called linear regression modeling can correct for this observed bias. This work will enable researchers to more accurately study patient brain tissue samples for pathologic proteins.
Simon Miller, University of Pennsylvania (class of 2020) & Felicia Cooper, Penn State College of Medicine (class of 2020)
Simon and Felicia worked together this summer to identify differences in pathologic tau protein between 40 “amnestic AD” patients who had memory problems during life and 40 “non-amnestic AD” patients who did not have memory problems during life. Specifically, they measured how much misfolded tau protein was present in 4 brain regions commonly affected in patients with AD: hippocampus, superior temporal gyrus, angular gyrus and mid-frontal cortex. Their results indicated patients with amnestic AD had greater misfolded tau protein in the hippocampus, a brain region important for memory compared to patients with non-amnestic AD. Furthermore, they found that patients with non-amnestic AD had greater misfolded tau protein in the temporal gyrus, angular gyrus and mid-frontal cortex, brain regions important for cognitive function but not specific to memory function. This work showed that non-amnestic AD and amnestic AD symptoms are associated with a different distribution and amount of the misfolded tau protein in the brain.