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Graduate Students:

 
     
Former Graduate Students:

 

Lani Clinton:

B.A., Williams College, Williamstown, MA 2002

lanikai@uci.edu

I was born and raised in Honolulu, Hawaii with my mom (Kathy), dad (Larry), brother (Nathan, 10), and sister (Tahnee, 14). After a frigid four years in Williamstown, MA for college, I have returned to sunny southern California to pursue my studies in graduate school. No more snowy winters, thank you. I have always loved science and when I discovered neuroscience in college, I was instantly hooked. The LaFerla lab is an extremely diverse and intellectually stimulating environment to work in. It is truly on honor to be a graduate student in this lab where we get to use state-of-the-art equipment and are on the cutting edge of Alzheimer’s research. My thesis project is to generate a transgenic model with the two hallmark lesions of Alzheimer’s disease, plaques and tangles, in addition to Lewy bodies (the hallmark pathological feature of Parkinson’s disease). A high percentage of Alzheimer’s patients have Lewy bodies in addition to plaques and tangles. Therefore, examining the interaction between all three protein aggregates in vivo is very intriguing and clinically relevant.

In my free time I like to play with my horse, Bender.

 

 

Debbi Ann Henderson:

B.S., Framingham State College, Framingham, MA 2000

Background:
I have always loved science, and when my grandmother was diagnosed with Alzheimer’s disease in 1985, and as I watched her slowly disappear amidst an onslaught of plaques and tangles, I decided to direct my love of science toward AD research. After obtaining my B.S. in Biology from Framingham State in 2000, I went on to study the AD vaccine in a double transgenic (APP/PS1) mouse model of AD in Dave Morgan’s lab at the University of South Florida (in Tampa, Florida) as a graduate student. In 2001, I took a hiatus from graduate school to start a family here in southern California. While my daughter was still an infant, I balanced being a stay-at-home mom with working part-time as a technician in Leon Thal’s lab at the University of California, San Diego. There I studied the effects of nerve growth factor on proliferation and migration of satellite cells (a type of glial cell) in the dorsal root ganglia of rats. In 2003, I resumed my career as a graduate student here at UCI. I am very excited to be continuing my quest to understand the disease that destroyed my grandmother (sadly, she spent the last 5 years of her life in a vegetative state –unable to speak, barely able to move- before finally passing away in the fall of 2003). I feel very lucky to again be working with the current top AD animal model (Salvo’s triple transgenic mouse).

Research:
No animal model to date has been able capture all 3 human pathological hallmarks of AD -plaques, tangle, and ultimately, neuronal cell death. The neuronal cell death aspect of AD has so far been the most elusive in mouse models, even though the cell death seen in human AD may indeed be the immediate cause underlying behavioral problems. My main focus in the lab is in determining the extent of cell death (if any) in the triple transgenic model and using cross-breeding strategies to increase neuronal cell death based on strain differences in susceptibility to excitotoxic cell death. In my free time (full-time grad student + mom = free time?) I enjoy sleeping and drinking coffee.

 

 

Micheal Sy:

 

Bert Tseng:

A.B., Harvard University 1997

btseng@uci.edu

M.D./Ph.D. Student

I was born in the mid-70s in the state of Georgia but I can't say that I recollect the place as we only lived there for a year. I spent my early childhood in a suburb of Boston, after a few years in a suburb of Chicago, before moving to fair Fresno, CA. There I remained until I graduated from high school and took flight to Harvard. My father once quipped that if he had known that I wanted to go to Harvard, we wouldn't have moved from Massachusetts. Apparently he thought that I would follow my older sister to Berkeley. I somehow managed to journey along a similar career path as she's training to become an ophthalmologist whereas I plan on becoming a physician-scientist. My first summer in college was filled with research on clathrin subunits. The next summer and the remainder of my college days drifted away in the lab of Dr. John Maggio where I became rather familiar with the beta-amyloid peptide. After graduating from college with a degree in physics, I took the next logical step and continued conducting research on Alzheimer's disease in the distinguished lab of Dr. Dennis Selkoe at the Brigham Woman's Hospital in Boston. During those two years, I applied to and was accepted by the UCI MSTP. Thus I returned to California. At UCI, I joined the LaFerla lab where I have managed to use RNA interference to knockdown APP expression in cell culture. In my free time, I try to lead an active life by playing tennis, volleyball, softball, basketball, or whatever activity my friends and I feel like engaging in. When I'm not being active, I enjoy having my ACL recontructed time and time again. Besides perusing journal articles, I find intellectual stimulation in a good physics, math or medical text and an occasional science fiction novel. Lastly, I manage to regress back to my adolescence from time to time by escaping into fanciful worlds created by my Gamecube.

 

Tritia Yamasaki:

no notes yet!

 

 

 

 

 

 

 

 

Former Graduate Students:

Malcolm A. Leissring, Ph.D.

mleissring@rics.bwh.harvard.edu

Ph.D., 2000 Department of Neurobiology and Behavior, UCI

Dissertation Project: Modulation of calcium signaling by presenilin mutations .

Awards: Edward Steinhaus Memorial Award for Excellence in Graduate Teaching (2000); Redfield Memorial Graduate Scholarship in the Molecular Biosciences (1999); Glenn Foundation/AFAR scholarship (1998)

Current Position : Postdoctoral Researcher, Center for Neurologic Disorders, Harvard University (Dr. Dennis Selkoe, advisor)

 

 

Michael C. Sugarman

msugarma@uci.edu

B.S., Union College, 1997

Dissertation Project: Transgenic mouse model
of inclusion body myositis

Awards: Glenn Foundation/AFAR Scholarship
(2000); Union College, Magna Cum Laude (1997).

 

 

 

 

 

Yama Akbari:

B.S., UCLA 1996

yakbari@uci.edu

Dissertation Project: Modulation of beta-
amyloid production by calcium signaling
pathways

Awards: Glenn Foundation/AFAR Scholarship
(2000); Phi Beta Kappa; Summa Cum Laude UCLA

M.D./Ph.D. Student

I was raised in Denver until early high school, when I moved to a Philadelphia suburb, then moved to Anaheim (Disneyland), California. I graduated high school in Anaheim and matriculated at UCLA in 1992 with the intention of becoming a physician. After conducting research first in opthalmology (Jules Stein Eye Insitute) and later in neuroscience, I realized that neuroscience stimulates me the most. Thus I conducted an honors thesis in psychobiology with Dr. Michael Fanselow on the neural basis for Pavlovian conditioning in the amygdala. During my thesis research, I realized that I truly enjoy research, and wanted to incorporate it into my future medical career. Consequently, I decided to pursue a combined MD/PhD program, and chose UCI because of the superb neuroscience reputation. Upon completing the first two years of medical school, I began conducting research in Dr. Frank LaFerla's lab and enjoyed it considerably. Frank's lab had a friendly and bright atmosphere conducive to successful scientific research.

My research revolves around the role of intracellular calcium dyshomeostasis in Alzheimer's disease. Since I've joined the lab, we've shown that calcium signaling is modified by both presenilin and amyloid precursor protein (APP). We were the first group to demonstrate that mutations in presenilin cause deficits in capacitive calcium entry and levels of endoplasmic reticulum stores. More recently, we showed that APP's intracellular fragment, which migrates to the nucleus and may effect transcription, also regulates calcium signaling. The latest fascinating data we've obtained involves the modulation of beta-amyloid production by calcium signaling, that is, that calcium signaling may lie upstream of beta-amyloid production, and that one can change levels of beta-amyloid by changing various intracellular pathways involved in calcium signaling.

Upon compeletion of my PhD, I will finish the remaining two years of medical school and perhaps pursue an academic career in neurology.


In my spare time, I like playing music (keyboard instruments, and Indian Tabla drums), playing intramural sports (football and basketball), working out, and going out.

 

 

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