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--></style><title>Biology Advanced Undergraduate
Seminars</title></head><body>
<div><font color="#000000">Dear Biology undergraduates:</font></div>
<div><font color="#000000"><br></font></div>
<div><font color="#000000">Please take note of the following
information from Prof. Horvitz on the Biology Advanced Undergraduate
Seminars.</font></div>
<div><font color="#000000"><br></font></div>
<div><font color="#000000">Best wishes,</font></div>
<div><font color="#000000">Janice</font></div>
<div><font color="#000000"><br></font></div>
<div><font color="#000000">*******</font></div>
<div><font color="#000000"><br></font></div>
<div><font color="#000000">TO: Biology
Majors</font></div>
<div><font color="#000000">FROM: H. Robert Horvitz,
Professor of Biology</font></div>
<div><font color="#000000"><br></font></div>
<div><font color="#000000">I am writing to inform you of an exciting
course offering from the Department of Biology for the 2005-2006
academic year: a set of 14 new and very current seminar courses,
7.340-7.346, Advanced Undergraduate Seminars. A complete list of
the courses, instructors, and brief course descriptions are enclosed.
The topics are highly varied and encompass areas of genetics,
biochemistry, molecular biology, structural biology, cell biology,
developmental biology, virology, aging, evolution, and human disease.
A student can take any number of these courses. The courses,
which generally involve four to eight students, are for 6 units,
graded pass/fail, and meet two hours each week. The focus is on
reading and discussing the primary research literature. Most
courses have two short written assignments. Some include field
trips to MIT research laboratories or to commercial sites using
technologies discussed in the courses. The level of each course
will be tailored to the students who enroll. Because of the
small size of these courses, we expect students not to drop these
courses once they have begun.</font></div>
<div><font color="#000000"><br>
These courses offer a number of special features: small class
size, a high degree of personal contact with the instructor, a focus
on the primary research literature, and an opportunity to discuss
current problems in biology interactively. I believe these
courses greatly enrich an undergraduate's experience. There are
limited alternative opportunities available to undergraduates to
interact closely with instructors who are experienced full-time
researchers; to learn to read, understand, and analyze primary
research papers; and to engage in the type of stimulating discussions
and debates that characterize how science is really done. Most
advanced MIT undergraduates (generally juniors and seniors) have been
sufficiently exposed to the basics of biology to be able to read the
primary literature and appreciate both methodologies and cutting-edge
advances. These courses have two goals: first, to expose
students to the kind of thinking that is central to contemporary
biological research; and second, to impart specific knowledge in
particular areas of biology. These courses are designed to be
intellectually stimulating and also to provide excellent preparation
for a variety of future careers that require an understanding both of
what modern biology is and of how it is done. Students who have
taken Advanced Undergraduate Seminars in the past (different specific
courses, same general design) have been enormously enthusiastic about
their experiences.<br>
<br>
I am writing to you before Registration Day to encourage you to
consider enrolling for one of these seminar courses. Please feel
free to contact any of the instructors to learn more about their
courses.</font><br>
</div>
<div><font color="#000000">To learn more about the Advanced
Undergraduate Seminars to be offered during both the Fall 2005 and
Spring 2006 semesters, please check our website (</font><font
color="#0000FF"><u>http://mit.edu/biology/www/undergrad/adv-ugsem.html</u
></font><font color="#000000">), join the instructors for the seminars
at a poster session on Registration Day, Tuesday, September 6 from
1-3pm in the Biology Building (68) lobby, and/or contact the
instructors directly.</font></div>
<div><font color="#000000"><br></font></div>
<div><font color="#000000"><br></font></div>
<div><font color="#000000">***</font></div>
<div><font color="#000000"><br></font></div>
<div><br></div>
<div><font color="#000000"><u><b>FALL 2005-2006<br>
<br>
</b></u><b>7.340 Nano-life: An Introduction to Virus Structure
and Assembly</b></font></div>
<div><font color="#000000">Instructors: Melissa Kosinski-Collins
(</font><font color="#0000FF"><u>kosinski@mit.edu</u></font><font
color="#000000">, 2-1876; HHMI Education Group), Peter Weigele
(</font><font color="#0000FF"><u>pweigele@mit.edu</u></font><font
color="#000000">, 3-3545; laboratory of Jon King)<br>
Fall 2005. Wednesdays, 11 am - 1 pm. Room 68-151.<br>
<br>
Watson and Crick noted that the size of a viral genome was
insufficient to encode a protein large enough to encapsidate it and
postulated that a virus shell is composed of multiples of identical
relatively small subunits. Today, high-resolution structures of virus
capsids reveal the products of such genetic economy to be highly
symmetrical structures, much like a geodesic dome composed of protein
subunits. Structures determined by X-ray crystallography and
reconstructions from cryo-electron micrographs combined with data from
traditional molecular approaches are beginning to reveal how these
nano-structures are assembled. In this course, we will discuss basic
principles of virus structure and symmetry, capsid assembly,
strategies for enclosing nucleic acid, proteins involved in entry into
and exit from cells, and the life cycles of well understood pathogens
such as HIV, influenza, polio, and herpes. We will also review
cutting-edge methods of structural biology and will participate in a
visit to the Department of Biology's transmission electron microscope
(TEM).</font></div>
<div><font color="#000000"><br>
<b>7.341 Not Just a Bag of Enzymes: DNA Dynamics in the Tiny
Bacterial Cell</b></font></div>
<div><font color="#000000">Instructors: Melanie Berkmen
(mberkmen@mit.edu, 3-6702; laboratory of Alan Grossman), Lyle Simmons
(simmon57@mit.edu, 3-3745; laboratory of Graham Walker)<br>
Fall 2005. Tuesdays, 11 am - 1 pm. Room 68-151.<br>
<br>
Bacteria were among the first organisms to inhabit the earth, and they
will probably be the last. While some bacteria are the causative
agents of diseases such as anthrax and cholera, other bacteria play
helpful roles, e.g., in plant development and antibiotic production.
Studies of bacteria have been important in the understanding of
central biological principles. For example, all cells possess
mechanisms that ensure that each daughter cell inherits a full
complement of genes after cell division. In humans, improper
chromosome segregation may lead to cancer or other diseases. In
bacteria, failed chromosome segregation results in death. Many
bacteria must also segregate relatively small DNA molecules called
plasmids, which can encode antibiotic-resistance and virulence genes.
In this course, we will investigate the molecular mechanisms by which
bacteria ensure the faithful segregation of their chromosomal and
plasmid DNAs. For example, to ensure proper DNA segregation, some
bacteria use an apparatus similar to that used for mitosis in
eukaryotic cells. If a chromosome inadvertently gets trapped between
daughter cells, a DNA pump is assembled at the site to help move the
DNA to its correct destination. Fluorescence microscopy has played a
pivotal role in studying the protein and DNA choreography involved in
plasmid and chromosome maintenance. We will visit an MIT research
laboratory focused on bacterial chromosome dynamics, and students will
experience first-hand several fluorescent microscopic techniques used
in this type of research. In addition, the class will tour the
Novartis Institutes for Biomedical Research in Cambridge and meet the
Novartis project leader in microbiology and infectious diseases.<br>
<br>
<b>7.342<x-tab> </x-tab>Evolution of the X, Y and Other
Sex Chromosomes<br>
</b>Instructor: Jennifer Hughes (</font><font
color="#0000FF"><u>jhughes@wi.mit.edu</u></font><font
color="#000000">, 8-8420; laboratory of David
Page)</font></div>
<div><font color="#000000">Fall 2005. Tuesdays, 1-3 pm.
Room 68-151.</font><br>
</div>
<div><font color="#000000">You may have heard the rumor that the human
Y chromosome is heading towards extinction or that the X chromosome is
a repository for most of our "brainy" and "sexy"
genes. While evidence is mounting to dispel such rumors, there
is clearly a fascination in the popular press and the general public
with the sex chromosomes. They are unique components of our
genomes, because of their sex-specific distribution: females have two
X chromosomes, while males have an X and a Y. The Y chromosome
has taken on the primary role in male sex determination and, as a
consequence, has become specialized over hundreds of millions of years
of evolution to become a concentrated center for sperm-production
factors. The sex chromosome system that we share with all
mammals has been well characterized but is only one example of a
tremendous variety of systems that are found in nature. In
this class, we will explore the diversity of sex-determining
mechanisms, with a focus on chromosomal systems and their evolution,
ranging from the familiar (XX<i> female</i> - XY<i> male</i> in
mammals and ZZ<i> male</i> - ZW<i> female</i> in birds) to the bizarre
(10 Xs<i> female</i> - 5 XYs<i> male</i> in the duck-billed
platypus). Despite this diversity, the evolution of sex
chromosomes appears to follow a strikingly similar path across
lineages as diverse as humans, birds, and insects: the member of the
sex chromosome pair that is present in only one sex degenerates over
time, losing the majority of its genes and shrinking in size. We
will learn about the evolutionary theories that attempt to explain
this degeneration, study experimental systems that allow these
theories to be tested, and discuss the influences of such factors as
lifespan, generation time, and even mating behavior.<br>
<br>
<b>7.343 A Love-Hate Relationship: Cholesterol in Health and
Disease<br>
</b>Instructor: Ayce Yesilaltay (</font><font
color="#0000FF"><u>ayce@mit.edu</u></font><font color="#000000">;
3-8802; laboratory of Monty Krieger)<br>
Fall 2005. Thursdays, 3-5 pm. Room 68-151.</font></div>
<div><font color="#000000"><br>
After World War II, a new mysterious epidemic was killing men over 55
like never before. To find out what was happening, researchers
focused on a small town in Massachusetts and started the largest and
longest epidemiological study of its kind. Our lives have not
been the same since. The results from the Framingham Heart Study
linked a person's blood cholesterol levels to the risk of having heart
disease, the number one killer in western industrialized societies
today. How could a small molecule like cholesterol, a major
constituent of our cell membranes, be to blame? In this class,
we will examine cholesterol's role in the cell and in the body as a
whole, from its function as a structural component of the membrane to
its function in signaling. We will learn that every cell is
faced with a choice either to make cholesterol or to take it up from
circulating blood. How does a cell know how much cholesterol is
inside it? We will talk about the transcriptional and
post-transcriptional mechanisms of cholesterol sensing and of feedback
regulation in cells. We will discuss cholesterol in the brain
and in the circulation, "good cholesterol" and "bad
cholesterol" and how they are taken up and used in cells.
We will consider what happens when cholesterol regulation goes awry in
cholesterol-related human disorders and in animal models of such
disorders. We will learn how the drugs that deal with some of
these disorders were discovered, their targets and current strategies
for discovering better drugs in the future.<br>
<br>
<b>7.344 Lost in Translation: From Egg to Embryo and
Beyond</b></font></div>
<div><font color="#000000">Instructor: Leah Vardy (</font><font
color="#0000FF"><u>vardy@wi.mit.edu</u></font><font color="#000000">,
8-5246; laboratory of Terry Orr-Weaver)</font></div>
<div><font color="#000000">Fall 2005. Thursdays 11 am -1 pm.
Room 68-151.<br>
<br>
Have you ever wondered how an egg becomes a fly, a frog, a mouse or a
human? Why heads are heads and tails are tails? While we look so
different from the humble toad, given that we both use many of the
same processes to develop. What lies at the heart of development
includes not just our genes, but also how these genes are
expressed,<i> i.e</i>., how mRNA is regulated. In this course we
will explore some of the ways in which mRNA is regulated and see the
developmental consequences when translation of mRNA into protein is
disrupted. We will consider flies, frogs and mice to see how they turn
on and off different mRNAs to meet their developmental needs. Topics
will include mRNA localization, which is fundamental in distinguishing
the head from the tail of a fruit fly. We will look at the importance
of protein translation in the maturation of frog and mouse eggs and in
the production of sperm and eggs in a hermaphrodite worm. We will
discuss the variety of ways an embryo can fine-tune its mRNA
expression to ensure production of a protein in the exact space and at
the exact time required. Examples will include different ways to
activate and suppress translation, including polyadenylation, the
action of specific RNA-binding proteins and the recently discovered
important role played by microRNAs. Finally, we will see that
misregulation of translation plays a central role in a number of human
diseases. <br>
<br>
<b>7.345 Diabetes and Obesity: Energy Balance and Disease<br>
</b>Instructor: Kelly Wong (kwong@wi.mit.edu, 8-0377; laboratory
of Harvey Lodish)<br>
Fall 2005. Thursdays, 1-3 pm. Room 68-151.<br>
<br>
Do you know how your eating behavior is controlled at the molecular
and cellular levels? How do the cells in your body determine how
much energy they need? What mechanisms does your body activate
to burn fat? Importantly, what happens when these processes go
wrong, leading to diabetes and obesity? Diabetes and obesity
constitute one of the fastest growing epidemics in the United States.
According to the U.S. Center for Disease Control, over the last 10
years there has been an alarming increase in the number of patients
diagnosed with diabetes and/or obesity across the United States.
The burden on the healthcare system imposed by diabetes was estimated
to be $92 billion dollars of direct medical costs in 2002. In
this course, we will discuss insulin, its signal transduction and the
sensitivity and resistance of muscle to the actions of insulin.
We will study the AMP-activated protein kinase, a master sensor of
cellular energy status. We will also examine the actions of the
hormone leptin and its role in controlling body weight and feeding
behavior, as revealed by studies of genetically engineered mouse
models. Besides leptin, other adipose tissue cytokines such as
adiponectin will be discussed. Finally, we will examine the
molecular consequences of beneficial activities, such as exercise, and
discuss pharmacological agents that are currently being used to treat
patients with Type II diabetes.</font></div>
<div><font color="#000000"><br>
<b>7.346</b> <b> RNA Editing from A to I</b></font></div>
<div><font color="#000000">Instructors: Ben Wong (</font><font
color="#0000FF"><u>bwong@mit.edu</u></font><font color="#000000">,
3-4704; laboratory of Alex Rich), Alekos Athanasiadis (</font><font
color="#0000FF"><u>alekos@mit.edu</u></font><font
color="#000000">,</font><font color="#0000FF"><u>
alekosathanasiadis@hotmail.com</u></font><font color="#000000">,
3-4704; laboratory of Alex Rich)<br>
Fall 2005. Wednesdays, 1-3 pm. Room 68-151.<br>
<br>
Being human takes only about 30,000 genes, being a fruitfly takes
about 14000 genes and being a yeast takes about 5-6,000 genes. Many of
these genes are highly similar among these and other species. How is
such wide range of organismal complexity achieved from a largely
similar set of basic genes? This question has become central in
molecular biology since the revealing of genome sequences a few years
ago. One answer to this question appears to lie in mechanisms that
allow single genes to encode a large number of variant products
(usually proteins). In contrast to the classic hypothesis that one
gene encodes one protein, post or co-transcriptional modifications of
messenger RNA often allow single genes to generate hundreds or even
thousands of proteins tailored to specific needs of the cells in
different tissues or at developmental stages. RNA editing by dsRNA
adenosine deaminases (ADARs), which convert adenosine to inosine, is
one mechanism that generates RNA diversity present in organisms as
diverse as primates and insects. In organisms as evolutionary diverse
as nematode roundworms and humans, RNA editing has a particular role
in the the central nervous system, altering the properties of
neurotransmitter receptors and ion channels. Abnormalities in these
activities have linked RNA editing to some of the most challenging and
mysterious diseases, such as schizophrenia, depression and epilepsy.
In addition, while useful for cells in fine-tuning protein and RNA
functions, RNA editing also can combat viruses by altering their
genomes and messages in a way that destroys information needed for
their replication and function. During this course we will study
ADARs, the enzymes responsible for A-to-I RNA editing, focusing on
ADAR biochemistry and structure. The study of the known substrates of
ADARs, mostly brain ion channels, will show us how editing modulates
function. We will also discuss computational methods for identifying
new ADAR substrates and the role that ADARs may play in molecular
evolution.<br>
<br>
<u><b> <br>
SPRING 2005-2006<br>
<br>
</b></u><b>7.340 Molecular Mechanism of Aging<br>
</b>Instructors: Danica Chen (</font><font
color="#0000FF"><u>danicac@mit.edu</u></font><font color="#000000">,
2-4140; laboratory of Lenny Guarente), Agnieszka Czopik (</font><font
color="#0000FF"><u>czopik@mit.edu</u></font><font color="#000000">,
3-3567; laboratory of Lenny Guarente)<br>
Spring 2006. Thursdays, 1-3 pm. Room 68-151.<br>
<br>
Aging is a degenerative process that results in decreased viability
and increased susceptibility to diseases. This course will focus on
molecules and molecular pathways that regulate the aging process, such
as the insulin-signaling pathway and members of the Sir2 gene family.
We will discuss the molecular mechanism of calorie restriction, the
only known dietary regimen that extends the lifespans of a variety of
organisms. Other topics will include the human premature aging
disorders Werner's Syndrome and Hutchinson-Gilford Progeria, the role
of oxidative damage and the mitochondria in aging, and the effects of
metabolism on aging. We will explore the reciprocal effects of aging
and immunity at the cellular and molecular levels and the ways these
effects may be relevant to human biology. The class will be concluded
with tours of a research laboratory at MIT and a biotech company both
focused on aging.<br>
<br>
<b>7.341. Virus-Host Interactions: A Molecular Arms Race Important for
Cell Biology and Disease<br>
</b>Instructor: Richard Jenner (rjenner@wi.mit.edu, 8-7181;
laboratory of Rick Young)<br>
Spring 2006. Tuesdays 3-5 pm. Room 68-151.<br>
<br>
Viruses are tiny genetic entities that lie in between living and
non-living things. Consisting of DNA or RNA protected in a protein
shell, viruses are inert until they come alive inside a host cell.
Viruses travel lightly with very few proteins and genes, instead
hijacking cellular proteins to replicate themselves. The cell responds
with an armament of antiviral proteins, attacking many aspects of
viral replication. Viruses in turn express specialized proteins that
act to block this host antiviral response. During this course, we will
examine multiple examples of this molecular arms race between virus
and host. We will learn about viruses that remain undetected within
cells and the thousands of viral elements that we all carry within our
genomes. We will also discuss how the battle between viruses and human
cells causes diseases such as AIDS and cancer and what the study of
virology teaches us about normal cellular functions.</font></div>
<div><font color="#000000"><br>
<b>7.342 The RNA Revolution</b></font></div>
<div><font color="#000000">Instructors: Rickard Sandberg
(sandberg@mit.edu, 3-7039; laboratory of Chris Burge), Michael Stadler
(stadler@mit.edu, 3-7039; laboratory of Chris Burge)</font></div>
<div><font color="#000000">Spring 2006. Thursdays, 3-5 pm.
Room 68-151.<br>
<br>
Recent findings have revolutionized our view of the roles of RNA in
biology. For example, short non-coding RNAs (microRNAs and short
interfering RNAs) play key roles in development and cancer by
regulating gene expression. The biology of short non-coding RNAs and
their importance in these processes will be topics for this course. In
addition, the mechanism of alternative splicing explains in part how
humans can express 500,000 different proteins with only 25,000 genes.
Alternative splicing, the process by which exons are joined in
different combinations to generate multiple variants of a gene, is
estimated to affect about 75% of all human genes. We will discuss how
alternative splicing diversifies the human protein repertoire,
influences sex determination and courtship behavior in fruit flies and
when disrupted can cause diseases such as spinal muscular atrophy.
Attention will also be given to catalytic RNAs that act in the
ribosome during protein synthesis. In each session we will critically
evaluate both the experimental and the computational techniques used
in the primary literature to foster an understanding of their
strengths and limitations. This course will give you an overview of
the exciting newly emerging roles for RNA.<br>
<br>
<b>7.343 Takin' Out the Trash: Quality Control in Cellular
Processes</b></font></div>
<div><font color="#000000">Instructors: Peter Chien (</font><font
color="#0000FF"><u>pchien@mit.edu</u></font><font color="#000000">;
laboratory of Tania Baker), Eric Spear (</font><font
color="#0000FF"><u>espear@mit.edu</u></font><font color="#000000">;
laboratory of Chris Kaiser)</font></div>
<div><font color="#000000">Spring 2006. Wednesdays, 3-5 pm. Room
68-151. <br>
<br>
Messenger RNAs are synthesized from a DNA blueprint, the proteins
resulting from these messages are produced using the complex machinery
of the ribosome, and finally these proteins must attain their proper
mature folded state. Although this process is extraordinarily
accurate, care must be taken by the cell to cope with the inevitable
mistakes that occur along this long and complicated pipeline. To
this end, the cell has evolved a broad range of mechanisms to ensure
the quality of the final protein product. For example,
improperly folded proteins are often recognized as aberrant and
subsequently degraded, relieving the cell of the potentially
detrimental effects of a non-functional and abnormal protein. In
this class, we will discuss some of the many mechanisms used for
cellular quality control. We will consider the stresses that can
generate such aberrant protein products and how the cell continuously
fights these challenges. The recognition of misfolded proteins
and how these proteins are targeted to the degradative machinery will
also be discussed. We will consider both prokaryotic and
eukaryotic quality control, drawing attention to the similarities
between these two systems as well as highlighting differences between
them. The importance of these quality control mechanisms will be
emphasized throughout the course by discussing a number of relevant
human diseases, including cystic fibrosis, Huntington's Disease, and
certain types of cancer.<br>
<br>
<b>7.344 Toxins, Antibiotics, Protein Engineering and the
Ribosome</b></font></div>
<div><font color="#000000">Instructors: Caroline Koehrer
(</font><font color="#0000FF"><u>koehrer@mit.edu</u></font><font
color="#000000">, 3-1870; laboratory of Uttam RajBhandary), Mandana
Sassanfar (</font><font
color="#0000FF"><u>mandana@mit.edu</u></font><font color="#000000">,
452-4371; Education Office)<br>
Spring 2006. Tuesdays, 1-3 pm. Room 68-151.<br>
<br>
What do the lethal poison Ricin,<i> Diphtheria</i> toxin, and the
widely used antibiotic tetracycline have in common? They all inhibit
protein synthesis by targeting the cell's translation machinery. Why
is Ricin such a powerful toxin? How does it work? If<i> Diphtheria</i>
toxin and tetracycline also inhibit translation, why do they have such
different consequences? How does resistance to antibiotics like
tetracycline arise? In this course, we will explore the mechanisms of
action of toxins and antibiotics that specifically target components
of the translational apparatus leading to the disruption of protein
synthesis. We will discuss the roles of these antibiotics and toxins
in everyday medicine, the emergence and spread of drug resistance, and
how we might overcome this increasing problem by identifying new drug
targets and designing new drugs. We will also discuss how the detailed
understanding of the structure of the ribosome and the translation
machinery has led to new technologies in protein engineering and
promising applications for human therapy.</font></div>
<div><font color="#000000"><br>
<b>7.345 Jellyfish, FRET and Quantum Dots: Illuminating
Biology with Fluorescent Probes</b></font></div>
<div><font color="#000000">Instructors: Andrew Dutton
(</font><font color="#0000FF"><u>adutton@mit.edu</u></font><font
color="#000000">, 2-2826; laboratory of Barbara Imperiali), Bianca
Sculimbrene (</font><font
color="#0000FF"><u>sculimbr@mit.edu</u></font><font color="#000000">,
2-2826; laboratory of Barbara Imperiali)</font></div>
<div><font color="#000000">Spring 2006. Wednesday 1-3 pm.
Room 68-151.<br>
<br>
Significant advances in biology have occurred through the use of
fluorescence techniques. The sensitivity and selectivity of
fluorescent probes has advanced our understanding of human diseases
and of many other areas of biology by allowing the study of proteins
within living cells. This course will focus on
fluorescence spectroscopy as a powerful probe to study biological
systems. We will first discuss fluorescence and methods to
fluorescently label biomolecules. Examples of the<i> in vitro</i>
chemical labeling of proteins and the hijacking of naturally-occurring
fluorescent proteins, such as GFP (a green fluorescent protein from
jellyfish), will be considered. Recent examples will be used to
demonstrate the power of fluorescence methods at the frontier of
biological research. We will learn how Fluorescence Resonance Energy
Transfer (FRET), quantum dots and single-molecule experiments have
impacted fields such as cancer biology and infectious disease. This
course will endow students with the ability to understand and
critically evaluate the primary literature, which is fundamental to
advanced careers in science and medicine. Fluorescence technologies
lie at the interface of chemistry and biology, and we hope that any
student interested in either of these areas will find the information
taught in this course extremely useful.</font><br>
</div>
<div><font color="#000000"><b>7.346 How Abnormal Protein Folding
Causes Alzheimer's, Parkinson's, Mad Cow and Other Neurodegenerative
Diseases</b></font></div>
<div><font color="#000000">Instructor: Atta Ahmad (</font><font
color="#0000FF"><u>giftee6@mit.edu</u></font><font color="#000000">,
3-3707; laboratory of Vernon Ingram)<br>
Spring 2006. Thursdays, 11 am - 1 pm. Room
68-151.</font><br>
</div>
<div><font color="#000000">The cause of both Alzheimer's Disease (AD)
and Parkinson's Disease (PD) is abnormal deposition of proteins in
brain cells. In addition, there are 20 other neurological diseases
caused by similar protein deposition. Millions of people suffer from
these diseases. The latest research shows that these diseases arise as
a consequence of a specific series of molecular events. First, a
protein assumes a non-native sticky "misfolded state." Two
or more such sticky proteins associate together to generate a multi
protein "oligomeric state." These oligomers can associate
with each other or can recruit newly formed sticky proteins, thereby
growing into bigger thread-like structures called "amyloid
fibrils." These fibrils can deposit either inside or outside
brain cells, disrupting normal biological functions and resulting in
neuronal cell death. Depending on the region of the brain affected,
this cell death leads to visible symptoms, such as memory loss, loss
of cognitive ability, abnormal muscular movements, involuntary shaking
and, in many cases, death. In this course, we will discuss the
processes that trigger protein aggregation (such as, mutations and
environmental effects) with an emphasis on Alzheimer's Disease,
Parkinson's Disease and Mad Cow Disease. The methods used to study the
processes of aggregation (<i>e.g.</i>, fluorescence spectroscopy,
circular dichroism, infrared spectroscopy, transmission electron
microscopy, confocal microscopy) will be discussed. We will consider
the consequences of the aberrant proteins on cellular processes. We
will also discuss potential targets for intervening with these
processes and approaches that could lead to possible treatments for
these disorders.</font><br>
</div>
<div><font color="#000000"><br></font></div>
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