[Bioundgrd] Fwd: Biology Advanced Undergraduate Seminars

Janice Chang jdchang at MIT.EDU
Wed Sep 7 22:22:24 EDT 2005


Dear Biology Undergraduates:

This is a reminder that the Biology department is offering the 
following undergraduate seminars during the fall semester.  The 
seminars are six-unit courses, graded pass/fail, and are open to 
sophomores, juniors, and seniors.

7.340  Nano-life: An Introduction to Virus Structure and Assembly
7.341  Not Just a Bag of Enzymes: DNA Dynamics in the Tiny Bacterial Cell
7.342  Evolution of the X, Y and Other Sex Chromosomes
7.343  A Love-Hate Relationship: Cholesterol in Health and Disease
7.344  Lost in Translation: From Egg to Embryo and Beyond
7.345  Diabetes and Obesity: Energy Balance and Disease
7.346 RNA Editing from A to I

If you have an interest in taking one of these seminars, but have a 
schedule conflict, please feel free to contact the instructors. Email 
addresses are below.  Times of classes can sometimes be rescheduled.

Sincerely,
Janice


>TO:     Biology Majors
>FROM:   H. Robert Horvitz, Professor of Biology
>
>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.
>
>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.
>
>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.
>
>To learn more about the Advanced Undergraduate Seminars to be 
>offered during both the Fall 2005 and Spring 2006 semesters, please 
>check our website 
>(http://mit.edu/biology/www/undergrad/adv-ugsem.html), 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.
>
>
>***
>
>
>FALL 2005-2006
>
>7.340  Nano-life: An Introduction to Virus Structure and Assembly
>Instructors:  Melissa Kosinski-Collins (kosinski at mit.edu, 2-1876; 
>HHMI Education Group), Peter Weigele (pweigele at mit.edu, 3-3545; 
>laboratory of Jon King)
>Fall 2005.  Wednesdays, 11 am - 1 pm.  Room 68-151.
>
>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).
>
>7.341  Not Just a Bag of Enzymes: DNA Dynamics in the Tiny Bacterial Cell
>Instructors:  Melanie Berkmen (mberkmen at mit.edu, 3-6702; laboratory 
>of Alan Grossman), Lyle Simmons (simmon57 at mit.edu, 3-3745; 
>laboratory of Graham Walker)
>Fall 2005.  Tuesdays, 11 am - 1 pm.  Room 68-151.
>
>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.
>
>7.342	Evolution of the X, Y and Other Sex Chromosomes
>Instructor:  Jennifer Hughes (jhughes at wi.mit.edu,  8-8420; 
>laboratory of David Page)
>Fall 2005.  Tuesdays, 1-3 pm.  Room 68-151.
>
>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 female  - XY male in 
>mammals and ZZ male - ZW female in birds) to the bizarre (10 Xs 
>female  - 5 XYs male 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.
>
>7.343  A Love-Hate Relationship: Cholesterol in Health and Disease
>Instructor:  Ayce Yesilaltay  (ayce at mit.edu; 3-8802; laboratory of 
>Monty Krieger)
>Fall 2005.  Thursdays, 3-5 pm.  Room 68-151.
>
>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.
>
>7.344  Lost in Translation: From Egg to Embryo and Beyond
>Instructor:  Leah Vardy (vardy at wi.mit.edu, 8-5246; laboratory of 
>Terry Orr-Weaver)
>Fall 2005.  Thursdays 11 am -1 pm.  Room 68-151.
>
>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.e., 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.   
>
>7.345  Diabetes and Obesity: Energy Balance and Disease
>Instructor:  Kelly Wong (kwong at wi.mit.edu, 8-0377; laboratory of 
>Harvey Lodish)
>Fall 2005.  Thursdays, 1-3 pm.  Room 68-151.
>
>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.
>
>7.346   RNA Editing from A to I
>Instructors:  Ben Wong (bwong at mit.edu, 3-4704; laboratory of Alex 
>Rich), Alekos Athanasiadis (alekos at mit.edu, 
>alekosathanasiadis at hotmail.com, 3-4704; laboratory of Alex Rich)
>Fall 2005.  Wednesdays, 1-3 pm.  Room 68-151.
>
>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.
>
>
>SPRING 2005-2006
>
>7.340  Molecular Mechanism of Aging
>Instructors:  Danica Chen (danicac at mit.edu, 2-4140; laboratory of 
>Lenny Guarente), Agnieszka Czopik (czopik at mit.edu, 3-3567; 
>laboratory of Lenny Guarente)
>Spring 2006. Thursdays, 1-3 pm.  Room 68-151.
>
>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.
>
>7.341. Virus-Host Interactions: A Molecular Arms Race Important for 
>Cell Biology and Disease
>Instructor:  Richard Jenner (rjenner at wi.mit.edu, 8-7181; laboratory 
>of Rick Young)
>Spring 2006. Tuesdays 3-5 pm. Room 68-151.
>
>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.
>
>7.342  The RNA Revolution
>Instructors:  Rickard Sandberg (sandberg at mit.edu, 3-7039; laboratory 
>of Chris Burge), Michael Stadler (stadler at mit.edu, 3-7039; 
>laboratory of Chris Burge)
>Spring 2006.  Thursdays, 3-5 pm.  Room 68-151.
>
>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.
>
>7.343  Takin' Out the Trash: Quality Control in Cellular Processes
>Instructors: Peter Chien (pchien at mit.edu; laboratory of Tania 
>Baker), Eric Spear (espear at mit.edu; laboratory of Chris Kaiser)
>Spring 2006.  Wednesdays, 3-5 pm. Room 68-151. 
>
>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.
>
>7.344  Toxins, Antibiotics, Protein Engineering and the Ribosome
>Instructors:  Caroline Koehrer (koehrer at mit.edu, 3-1870; laboratory 
>of Uttam RajBhandary), Mandana Sassanfar (mandana at mit.edu, 452-4371; 
>Education Office)
>Spring 2006. Tuesdays, 1-3 pm. Room 68-151.
>
>What do the lethal poison Ricin, Diphtheria 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 Diphtheria 
>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.
>
>7.345  Jellyfish, FRET and Quantum Dots:  Illuminating Biology with 
>Fluorescent Probes
>Instructors:  Andrew Dutton (adutton at mit.edu, 2-2826; laboratory of 
>Barbara Imperiali), Bianca Sculimbrene (sculimbr at mit.edu, 2-2826; 
>laboratory of Barbara Imperiali)
>Spring 2006.  Wednesday 1-3 pm.  Room 68-151.
>
>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 in vitro 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.
>
>7.346  How Abnormal Protein Folding Causes Alzheimer's, Parkinson's, 
>Mad Cow and Other Neurodegenerative Diseases
>Instructor:  Atta Ahmad (giftee6 at mit.edu, 3-3707; laboratory of Vernon Ingram)
>Spring 2006.  Thursdays, 11 am - 1 pm.  Room 68-151.
>
>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 
>(e.g., 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.
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