Q U a R T E R

EUROSCIENCE NSUMMER 2006 QUARTERLY “The times demand that SfN Celebrates Opening of Its New we as neuroscientists Headquarters Building in Washington constantly advocate for The Society for Neuroscience cel- the funding necessary to ebrated its new headquarters build- achieve the exciting break- ing and office space in Washington, DC, with an opening gala on May 5. throughs envisioned by the Approximately 150 guests attended, Roadmap and the Blue- including past presidents, representa- print, and enabled by the tives from the Spanish and Italian embassies, SfN committee chairs, Human Genome Project.” NIH directors, and other leaders in the sciences. — SfN President Stephen Heinemann The evening’s events began in the (see page 2) building lobby, where SfN President Stephen Heinemann welcomed at- Stephen Heinemann and Edward Perl, SfN’s first presi- tendees to the dedication ceremony. dent, cut ribbon, formally opening the building. I N T H I S I S S U E “This new building represents many things to the Society. Among the most important is that it embodies the vision and mission shared by all of SfN’s leaders,” said Heinemann. “This building is a sign that SfN Celebrates Opening .............................. 1 neuroscience and the Society are committed for the long term to supporting and Message from the President ....................... 2 playing a role in the research enterprise, and to maintaining a strong presence in our nation’s Capital.” Cajal Mural Dedication ............................... 4 Neuroscience 2006 ..................................... 5 Past President Carol Barnes, head of SfN’s Real Estate Committee, spoke about the environmentally responsible strategies behind the headquarters’ construction. “As Society Programs ........................................ 6 the chair of the Society’s real estate committee, I am very pleased that this building NIH Funding ................................................ 7 reflects the personal values of environmental responsibility that we as neuroscientists feel are important. It also serves as a visible symbol in our nation’s capital of the Q & A with James Collins ............................ 8 excitement of neuroscience — something about which all SfN members are very Publishing Open Access Group proud,” she explained. Seeks Member Comments ........................ 10 Heinemann and Edward Perl, SfN’s first president in 1969, then cut a ribbon, formally opening the building. A reception in SfN’s office space gave attendees an opportunity to tour the ninth through eleventh floors and chat with colleagues and SfN staff over drinks and hors d’oeuvres. Also, they were able to see and learn about the three-story, three-dimen- sional mural hanging in the space’s central stairwell (see article on page 4). The mural, dedicated at the gala by SfN President Stephen Heinemann, is based on a drawing of the mouse neocortex by Santiago Ramón y Cajal, who shared the Nobel Prize for Physiology and Medicine with Camillo Golgi in 1906. This year marks the Continued on page 15. Message from the President Bedside to Bench to Bedside: Redefining Clinical and Basic Science Research 2 Some basic scientists worry that characterized by loss of speech and constant hand-wring- funding is biased toward transla- ing. Within a few weeks, she had found seven patients tional research - focused only on with the disorder known as Rett syndrome. Two years curing disease rather than basic after first encountering patients with this disorder, Zoghbi science — creating an artifi- interrupted her clinical career for intense genetics train- cial tension between basic and ing in the hopes of understanding the causes of diseases clinical research. Rather, these like Rett syndrome. After establishing her lab in 1988, Stephen Heinemann, fields actually inform each other she began hunting for the gene on the X chromosome SfN President and are both important. This is and collected more than 200 patient samples. illustrated when scientists start with a human disease, look for a gene, then make animal In 1999, Zoghbi and her collaborators discovered that models and do experiments that result in treatments for Rett syndrome is caused by mutations in the gene encod- patients. Increasingly, clinical research and basic science ing methyl-CpG-binding protein 2 (MECP2) located on are converging. We should be mindful of this as we go the X chromosome. Studies now show that MECP2 is im- about our research, and think about the enormous prog- portant for synaptic plasticity. Furthermore, scientists are ress now possible through cross-fertilization. now beginning to find the gene’s targets which will help link molecules to specific neuronal function. Ultimately, A classic contemporary example of how the study of Zoghbi hopes to target these pathways to treat patients. human genetics informs basic science, and helps science Her talk is titled “Rett Syndrome and MECP2: Gateway understand and find better treatments for disease, is the to Postnatal Neuropsychiatric Disorders.” She’s a Howard story of Michael Brown and Joseph Goldstein, who won Hughes Medical Institute investigator at Baylor College of the Nobel Prize in Medicine or Physiology in 1985 for Medicine. their work on the cholesterol pathway. One of Zoghbi’s collaborators is another 2006 presiden- In studies of cultured cells of normal people and those tial lecturer. Harry Orr, a geneticist at the University of with inherited high cholesterol, Brown and Goldstein Minnesota, heads a team interested in unraveling genes found that the cells of patients with the most severe form that encode proteins critical for proper neuronal func- of the disease completely lacked functional low-density li- tion. His primary approach is to study genes that have poprotein (LDL) receptors. The underlying mechanism of a role in neurodegeneration. Orr studies the molecular severe hereditary familial high cholesterol was determined basis of spinocerebellar ataxia type 1 (SCA1), one of nine to be a complete, or partial, lack of functional LDL-re- polyglutamine disorders. SCA1 damages neurons in the ceptors, leading to increased levels of cholesterol in the brain’s cerebellum, resulting in a loss of muscle control. It blood which subsequently may accumulate in the wall of usually strikes during the prime of life, cruelly rendering arteries causing atherosclerosis and eventually a heart at- its victims unable to walk and speak before killing them tack or a stroke. Knowing this, statins were developed and within 10 to 20 years of onset. revolutionized the treatment of high cholesterol. The starting point for these genetic studies was the clini- The talks to be delivered by the four presidential lecturers cal characterization of the disease in patients by other at Neuroscience 2006 in Atlanta also will highlight how researchers. Orr employed an approach often called posi- the study of human genetics informs basic neuroscience tional cloning in which DNA was collected from and tells us more about human disease. In each case, re- 200 family members with the disease. Genetics were search is leading to therapies for devastating neurological used to determine the inheritance pattern. DNA markers disorders that now have no treatment. and linkage analysis then determined the chromosome and place where the gene is located. Molecular approach- In the fall of 1983 as a resident in child neurology, Huda es then cloned the gene. In this case, the cause of SCA1 Zoghbi began to notice in young girls an obscure disorder was found to be a mutation on a gene located on chromo- 3 some 6. Orr then made several mouse models for Five years ago, Carmeliet and his colleagues found that the disease that have helped to understand basic mutations in a gene known for triggering new blood ves- aspects of the disease process and normal function of sel growth were linked to symptoms much like amyotropic the protein _ findings that have led to the identification lateral sclerosis (ALS) in lab animals. Normally, the gene of potential therapeutic approaches. Orr’s talk is titled for vascular endothelial growth factor (VEGF) is respon- “Neurodegenerative Disorders: Linking Basic and sible for growth of new blood vessels. But the altered Clinical Neurosciences.” expression of the gene produced progressively weaker muscles and spinal cord injury similar to ALS. Studies of Sangram Sisodia of the University of Chicago will discuss some 2,000 people found three slightly different versions advances made through the study of the “Molecular of the gene which appeared to cause lowered levels of Neurobiology of Alzheimer’s Disease,” initially involv- VEGF protein in the body. What’s more, the low VEGF ing families in which the disease was inherited. The first levels corresponded with a higher risk of developing ALS. genetic studies conducted during the late 1980s showed genetic markers for the disease-causing beta-amyloid Recently, Carmeliet has shown that VEGF is critical to precursor protein (APP) on chromosome 21. Later, genes nervous system development. He is now exploring the known as presenilin 1 (PSEN1) and presenilin 2 (PSEN2) possibility of VEGF gene therapy for ALS. Preclinical were identified. animal studies have shown that this therapy can slow the onset of disease and increase life expectancy by 30 Although mutations in PSEN and APP genes are seen percent. Clinical trials are expected to start within a year. only in the relatively rare cases of familial Alzheimer’s that occur early, the symptoms and laboratory test features of As these examples show, the opportunity to turn clinical these individuals are indistinguishable from the larger AD genetics and basic science into new therapies is very real. population whose disease begins after the age 60. With And collaboration across disciplines — aided by emerging this in mind, Sisodia and others have focused their efforts technologies such as genomic mapping, increasingly sophis- on clarifying the dysfunction of mutant APP and presenel- ticated imaging tools, and animal models — is leading to in protein product variants in cellular models and in trans- profound insights into the nervous system and how it works.

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