Dr Lauren Billings Luhrs: |
I grew up in the San Francisco Bay Area
(Albany, specifically) but left CA to go to Macalester
College, a fantastic, small school in St. Paul Minnesota.
My interest in neurodegeneration, specifically in Parkinson’s
Disease, began while studying biology in college, and
was enhanced while working with adults with mental illness
and neurodegenerative disorders. After college I continued
to work with this population and I was struck by the
incredible vulnerability of the dopaminergic system,
both in terms of the side effects of antipsychotic drugs,
as well as the vulnerability of dopamine cells in Parkinson’s
Disease (PD). I realized that there was so much to be
learned about dopaminergic neurons as well as about
structures receiving dopamine innervation. I came to
UCI to do my graduate work with Dr. John Marshall studying
PD models and the effects of dopamine depletion in a
basal ganglia structure called the globus pallidus.
I had a fantastic time in the UCI Neurobiology and Behavior
program!
Throughout my work here, I’ve kept a keen eye
on Dr. LaFerla’s work. I finished my Ph.D. in
June 2003 and was thrilled to come work in the LaFerla
lab. While my graduate work was always been generally
classified as Parkinson’s Disease-related, Alzheimer’s
Disease has also fascinated me. Dr. LaFerla has often
referred to neurodegenerative diseases as existing along
a continuum, with purely cognitive disorders on one
end, and purely motor disorders on the other. It’s
amazing the extent to which these disorders intersect,
and I look forward to learning more about those common
processes.
My graduate work was more anatomical in focus, i.e.
what population of globus pallidus neurons are most
affected with a loss of dopamine tone, where do these
neurons project, what do they do and how is behavior
affected when dopamine is depleted in this region? In
Dr. LaFerla’s lab I’ll be learning molecular
techniques as well as expanding my behavioral testing
experience. I’ll be working with the 3xTg-AD (triple
transgenic Alzheimer’s Disease model) mice doing
behavioral testing and evaluation, and I’ll also
be studying the effects of cholesterol on the beta amyloid
and tau pathology in the 3xTg-AD mice.
When I’m not in lab, I love to play softball,
cook, read and travel. I have two kitties (Little Bear
and Maddie), a husband (Keith) and year-round good weather!
The LaFerla lab has a great group of people. If you
have any questions about the Neurobiology and Behavior
graduate program or about UCI in general, please feel
free to drop me an email!
Email: laurenb@uci.edu
no notes yet!
 One
of the Brits currently residing in Franks lab, I am
originally from Essex – a county 50 miles east
of London. I went to university in 1996 at the University
of Birmingham where I obtained a B.Med.Sci.
After that I began a PhD with Prof. Chris Peers at
the University of Leeds where I learnt to patch clamp.
I studied whole cell calcium currents and the effect
that chronic hypoxia had upon them. It turned out that
amyloid beta peptides (ABP) were deeply involved in
how calcium channels were being affected by the hypoxia,
both through Reactive Oxygen Species (ROS) generation
and through novel amyloid beta “channels”
which conducted Ca2+ and tightly couple to secretion
of catecholamine containing vesicles.
I finished my PhD at the end of September 2002 and
then jumped on a plane to India. I spent the next 6
months traveling round the jungles of asia and the pacific
before returning to sunny England and then jumping back
on a plane to California to start work for Frank.
I have been working on the physiological role of the
presenilins on cellular calcium homeostasis, along with
the effects of stress and glucocorticoids on Alzheimer's
pathology and also looking at a possible therapy for
Alzheimer's disease using dietary fatty acids.
Email: kngreen@uci.edu
 Research
interests: Muscle and neurodegenerative disorders
I was born and raised in Nagano, Japan. As you may recall
your memory (if you are not Alzheimer’s disease),
we had the Winter Olympic in 1998. It is a beautiful
city especially in snow. After high school in Nagano,
I came to California to complete B.S. in Biochemistry
and M.S. in Environmental Toxicology. Then, I moved
to Ames, Iowa to finish my Ph.D. in Toxicology. Everything
was great there, except I sometimes had to deal with
snow and worse weather, blizzards and storms. Yet, I
enjoyed a lot. After completion of my Ph.D., I again
moved back to California, where I am continuing my research
as a Post-doctoral researcher here at UCI.
My graduate research project was to investigate the
positive association of environmental chemicals with
the etiology of dopaminergic neurodegeneration and Parkinson’s
disease (PD). I characterized dopaminergic toxicity
of dieldrin (pesticide), methylcyclopentadienyl manganese
tricarbonyl (MMT, a gasoline additive), and manganese
with related to oxidative stress-mediated caspase-dependent
signaling cascades in dopaminergic cells.
Using my knowledge about cell biology and neurotoxicology,
I would like to pursue my research interests here in
LaFerla’s lab. One of my projects will be characterizing
the impact of metals in Alzheimer’s disease (AD)
pathology, namely b-amyloid (Ab) aggregation and tau
hyperphosphorylation. Significantly elevated brain concentrations
of copper, zinc and iron have been reported in AD patients,
and these metals are particularly localized in Ab deposits.
Cu and Fe are transition metals, and they are capable
of generating reactive oxygen species (ROS) via Fenton-like
reaction. We hypothesize that elevated metal concentrations
in brain and Ab plaques may be potential sources of
ROS generation, which further triggers oxidative stress-mediated
neurodegeneration. Assessing metal toxicity in relate
with AD using triple transgenic (PS1, APP, human tau)
mice model could not only answer the involvement of
metals in AD pathology, but also provide cellular and/or
molecular basis of new evidence for possible association
between Ab aggregation and tau hyperphosphorylation.
Revealing these pathological processes may help to develop
new therapeutic strategies for AD.
My another project, which is my primary project, is
to investigate the disease called inclusion body myositis
(IBM). IBM is a muscle disease, and the cause is not
yet fully understood. Mutations of some genes may be
involved in the pathogenesis of IBM. Interestingly,
Ab may be responsible for degradation of muscles. We
have generated transgenic mice expressing human APP
in skeletal muscles as a novel model of IBM. Using these
mice, we are currently characterizing the mechanism
of Ab accumulation and subsequent muscle degeneration.
Furthermore, crossing these mice with other genetically
modified mice to identify which gene(s) may play an
important role in the pathogenesis of IBM. We have an
excellent model and I hope it will help to discover
possible therapeutic strategies for IBM.
Email: kitazawa@uci.edu
 M.S.,
University of Catania,
Catania, 1999
Ph.D. University of California, Irvine, 2005
soddo@uci.edu
I grew up in Ferla, a small town of about 3,000 people,
that is located about 40 minutes west of Siracusa (Sicily,
Italy). I graduated cum laude from the University of
Catania with a specialization in molecular biology in
1999. I spent the last two years of my studies in Italy,
working on the cloning of a human voltage-dependent
anion selective channel. After I graduated, I joined
Prof. LaFerla's laboratory. Here I found a very well
equipped state-of-the-art laboratory and a very friendly
environment in which to work. Almost since day one,
I started working on a project to develop a novel transgenic
mouse model of Alzheimer's disease. I enjoy research
thoroughly and am going to apply for admittance into
the Neurobiology and Behavior graduate program here
at UCI. I am an avid soccer fan and enjoy playing it
on the weekend with the other international students
at UCI and also watching it on TV, which required that
I subscribed to an Italian TV channel. Ciao!
No notes yet!!
 I’m
a Brit from Liverpool, UK, working in Franks Lab. I
joined the lab in February of 2003 specifically to expand
and work on the Ca2+ hypothesis of AD.
My undergraduate life was spent with the Pharmacology
department at the University of Leeds (now Biomedical
Sciences). Whilst there, I had the opportunity to do
my final year research project with Pfizer Global Research
at Sandwich in Kent. My graduate work (sponsored through
a CASE award by Pfizer) was spent working under the
supervision of Chris Peers at the University of Leeds
where we were investigating the signaling pathways linking
why people whom suffered from a stroke (i.e. low O2
brain levels) were significantly more likely to go to
develop AD.
Recently, our lab here developed a triple-transgenic
model of Alzheimer's disease by introducing two additional
transgenes (APPswe and tauP301L) into the germline of
the PS1 mutant knock-in mouse. Animal models have proven
useful in studying the impact of mutant AD-related genes
on other cellular signaling pathways such as Ca2+ signaling.
Along these lines, disturbances of intracellular Ca2+
homeostasis are an early event in the pathogenesis of
AD. One of the projects I am involved with is determining
the impact of these genes on intracellular calcium signaling
and I am also collaborating with Jorge Busciglio’s
group here at UCI in the hope of gaining a further understanding
to the role that mitochondrial dysfunction plays in
Downs Syndrome. I have also had the opportunity to develop
and assist in other projects ongoing in the lab ranging
from the intracellular localization of Ab in the triples
through to testing the ability of novel compounds (in
collaboration with drug companies) to delay or promote
the pathology we see in our transgenic mice.
When not in the lab, I play football for Irvine City
FC (www.irvinecityfc.com).
Email: ismith@uci.edu
Ph.D., 1999, Neuroscience
New York University
grace@uci.edu
Research Interests :
Calcium signaling
Physiology of neurodegenerative disorders
Transgenic Models
My research interests over the past several years
have spanned across a few different scientific projects,
but have always been under the umbrella of studying
neuropathological disorders at the systems/cellular
level using electrophysiological and pharmacological
techniques. These have included studies of the amygdala
and its relation to stress (as a graduate student at
NYU with Joe LeDoux), and the modulation of serotonergic
activity in the prefrontal cortex to better understand
psychosis (at Yale University with George Aghajanian).
Here at UCI, I am expanding on this by combining molecular/transgenic
and functional imaging techniques to study the effects
of Alzheimer's disease (AD)-causing mutations on intracellular
calcium regulation. In order to combine the worlds of
cellular-molecular biology with electrophysiology/imaging
to answer these questions, I work with experts in each
of these fields. In Frank LaFerla's lab, we are generating
transgenic mouse models that will allow us to monitor
changes in neuronal calcium levels quickly and easily
across different AD-containing mutants. In Ian Parker's
lab, we are characterizing the dynamics of IP3 -mediated
calcium release from intracellular stores, and it's
effects on membrane excitability. This is accomplished
using a custom-built video-rate multiphoton imaging
system in conjunction with in vitro electrophysiological
slice recordings from mouse brains. LaFerla's lab has
shown that mechanisms related to IP3 -mediated calcium
release are altered in cell lines containing AD-causing
mutations. My research will explore this calcium dyshomeostasis
in functional neurons from transgenic mice, and attempt
to characterize the mechanisms and functional implications
of alterations in this pathway of neuronal calcium release.
When not playing with mice, or my dog Murphy, my cat
Pfinster, or my patient husband Manny, I can usually
be found playing softball (go Synaptic Sluggers!!) in
the spring/summer, skiing in the winter, running (when
motivated), or, my personal favorite, taunting my friends
and family back home in NY that I am out golfing during
their ice/snow/rainstorm (year-round). After 9/11, I
am glad they are all still there. I also serve as the
UC Irvine representative to the Council of Postdoctoral
Scholars, which is a recently formed committee attempting
to standardize and improve policies relevant to postdocs
throughout the entire UC system, and serve as a model
to universities nationwide (). If you have any comments
or suggestions, I'd love to hear them.
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