http://news.bmn.com/conferences/list/view?fileyear=2001&fileacronyn=SFN&pagefile=confsummary.html
21 November 2001
The Society for Neuroscience annual
meeting "is a zoo," one neuroscientist put it, some weeks before this year's
conference: "Everyone hates it, yet everyone goes."
This year was no different: Undaunted
by slashed budgets or security concerns, a record 28,500 attendees from
all over the world swarmed in on sunny San Diego.
Armed with massive programs, neuroscientists
could be seen and heard everywhere: in hotels, restaurants, on TV, in taxicabs,
jogging on the boardwalk. For the week of the conference, the town normally
known for such intellectual exclamations as "dude" and "sweet!" resounded
with animated debates on neuronal plasticity, synapses and signaling.
For some young scientists, the main
attraction was the opportunity to see neuroscience greats and Nobelists
like Eric Kandel, Stanley Prusiner and Paul Greengard. In a Presidential
Special Lecture Paul Greengard told a packed conference hall that the latest
studies of the dopamine receptor, implicated in disorders from Parkinson's
disease to schizophrenia, all converge on DARPP-32, a molecule he predicts
will make pharmaceutical companies very happy.
Stem cells, which dominated last
year's program, again made for memorable news. Glial cells, which most
neuroscientists have regarded as support cells, can in fact serve as stem
cells that generate neurons even in adults, Magdalena Götz and her
colleagues at the Max-Plank Institute of Neurobiology reported. Harvard
neurologist Evan Snyder proposed that transplanted neural stem cells can
alleviate neural degeneration by instructing host cells to regenerate,
rather than by maturing into neurons themselves.
One of the most intriguing studies
of the conference came from Arthur Craig of the Barrow Neurological Institute
in Phoenix, Arizona. Craig presented classic anatomical tracings, as well
as cutting-edge PET and fMRI scans, that delineate the insular cortex,
a unique region he says registers the inner state of the body and generates
the uniquely human sense of self.
Using such fancy imaging techniques
to reveal the workings of the brain was a common thread in this year's
sessions. Electron microscopy is poised to unravel the mysterious structures
within the nerve synapse, revealed Uel (Jack) McMahan, a professor of neurobiology
at Stanford University School of Medicine. Entire sessions were devoted
to new techniques in diagnosing Alzheimer's disease (AD), the most promising
of which is a derivative of the Congo Red probe that can penetrate the
blood-brain barrier and selectively label plaques, tangles, and cerebrovascular
amyloid.
University of Pennsylvania researchers
identified regions of the brain that become metabolically active when a
person lies, using used to identify event-related functional magnetic resonance
imaging (fMRI); Canadian researchers unmasked the connections between speech
and music, between listening and performing; and Emory University researchers
pinpointed a region that helps us grasp mirror images and use them to direct
our movement.
For the first time, researchers have
also been able to predict a monkey's behavior solely on the basis of which
neurons fire in a portion of its brain. Columbia University neurologist
Michael Goldberg arrived at those results using a novel test to measure
attention. SFN's president-elect Huda Akil is employing increasingly popular
microarrays to identify genes that are important in emotional response.
Cortical molecules of the stress system play a critical role in shaping
individual differences in emotional reactivity, Akil said.
Several different teams also presented
seemingly contradictory results on gender-specific differences in the response
to stress. Columbia University neurobiologist Darcy Kelley says the South
African clawed frog, Xenopus laevis may be a model system to study the
cellular effects of hormones in generating gender-specific characteristics.
Janis Weeks of the University of Oregon also showed precisely how steroid
hormones affect individual neurons in the simple nervous system of a caterpillar.
As with other years, several sessions
were devoted to individual disease studies. Two types of cell transplants
were shown to hold off muscle atrophy in mouse models of amyotrophic lateral
sclerosis (ALS). University of Pennsylvania researchers discovered that
dendrites, the signal-receiving end of neurons, go awry to cause diseases
such as Fragile X mental retardation. Scientists cautioned that the miracle
drug L-dopa, which has been prescribed for Parkinson's disease (PD) patients
for more than 30 years, may itself be partly responsible for the cognitive
deficits associated with PD. Alzheimer's disease researchers dueled over
the efficacy of the vaccine approach, now in clinical trials, in reversing
cognitive deficits associated with that disease.
In normal aging brains, the prefrontal
area of the brain takes the biggest hit, and people who age successfully
compensate for the loss by engaging both hemispheres. In neurodegenerative
diseases like AD and PD, some researchers argued, protein aggregates themselves
may not directly damage the nerve cells, or produce the clinical signs.
Rather, they suggest, dysfunction may be due to the toxic effects of soluble
forms of the affected proteins.
In neuroscience, perhaps more than
other life sciences, such disagreement is not uncommon. Synaptic research
veteran Thomas Sudhof rued his role in the "in-fighting" of the synapse
world, saying, "many times, scientists propose ideas not because they believe
it's completely true but to be known for an idea. It would be better to
concentrate on known facts." Dale Schenk, who took the contentious Alzheimer's
field by storm two years ago, advised young scientists to just worry about
the science. "You can't own science. It is what it is," he said. "Patients
don't care who did what when. All they care about is a treatment. And we
have to work as hard as we can do that."
SFN 2001
by Apoorva Mandavilli
Society for Neuroscience
© Elsevier Science Limited
2000