Stress and the Brain

Didn’t sleep well last night? Your immune system may be in overdrive today, starting or continuing a cascade of stressors that could spell ill for your body and brain.


Janice Kiecolt-Glaser

“If you didn’t sleep, if you had a tired night, your IL-6 levels are higher today,” said Janice Kiecolt-Glaser of Ohio State University. IL-6 (Interleukin 6) triggers inflammatory and auto-immune processes that protect the body, but too much response has been linked to such diseases as diabetes, atherosclerosis, lupus, arthritis, and anxiety and depression.

Kiecolt-Glaser stepped through several studies and reviews of research on immune reactions to stress during the forum “Stressing About Stress–What Our Minds and Bodies are Going Through and Ways to Cope” at the American Association for the Advancement of Sciences (AAAS) in Washington, DC, on Thursday.

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MIT Highlights Work of Dana Grantee J. Christopher Love

Last week, MIT released a new piece highlighting the work of Dana grantee J. Christopher Love, Ph.D. Dr. Love received a Dana grant in 2009 through one of the Foundation’s former programs, Human Immunology, for his project entitled Single-Cell Microtools for Profiling Human Immune Responses to HIV.

He and his colleagues have uncovered some important aspects about how T cells respond to HIV, which may help researchers develop an HIV vaccine in the future. Their research was first published in The Journal of Clinical Investigation.

–Caitlin Schneider

From the Archives: Ralph Steinman

When I woke up yesterday morning and turned on my radio, I was excited to find out that noted immunologist and long-time Dana consultant Ralph Steinman had won the Nobel Prize for medicine. What my colleagues and I did not discover until a few hours later was that Dr. Steinman had died three days earlier, four-and-a-half years after he was diagnosed with pancreatic cancer. Steinman

In honor of Dr. Steinman, the latest From the Archives feature is a profile of him written by Web Editor Nicky Penttila after he was awarded the prestigious Lasker Prize in 2007. Here is an excerpt about his early research:

In the 1970s, when Steinman started his research career, researchers knew about the "musician" cells and they knew about infections. But in their laboratories, they could not seem to energize the immune cells to react to the infections. A link was missing, some cell in the immune-system soup that flipped the immune system cells on, and on in the right direction. They called the cells they were looking for "accessory cells."

Steinman was working in the lab of the late Zanvil Cohn at Rockefeller University, an expert in the physiology of macrophages, which were considered to be a leading candidate for the missing accessory cells.  "We looked at the populations [of cells] that were the source of the accessory cells," Steinman says. Using spleen tissue from mice, "we found unusual cells that had never been seen before; they were tree-like in shape. Hence the name we gave them, dendritic, from the Greek word for tree."

You can also read Dr. Steinman’s columns from the 2007-2010 issues of Immunology in the News—no one could write about immunology more clearly than he could.

Dr. Steinman was a brilliant scientist, extraordinary communicator, and wonderful person. We will miss him.

–Johanna Goldberg

The uphill battle against HIV

An editorial this week in The Washington Post, “HIV/AIDS:
The Incurable Epidemic
,” cites disappointing results from two recent
studies. A separate press release from Duke University cites a “major roadblock”
in another
HIV study
. Simply put, the road to curing this virus continues to be an
uphill slog.

The first study the editorial mentions, the RV144 trial, was
hailed as a
back in September because it was the first trial ever to show
even “modest” protection against HIV infection. Many thought the results,
obtained from a set of Thai patients, suggested that a legitimate AIDS vaccine
would soon be in the making. Further analysis, however, showed that the results
were less dramatic than originally thought and may even be explained by a
statistical fluke. Though researchers maintain that the results are still important,
the new caveats strike a resounding blow against the possibility of a
commercial vaccine in the near future.

The results of the other study, which looked at a gel
designed to prevent HIV transmission to women, were released on Monday. Although
the compound, which was tested in more than 9,000 women in South Africa,
Uganda, Zambia, and Tanzania over four years, had shown early successes in the
lab and in small trials, it was a complete failure on a larger scale.

The Duke University researchers, meanwhile, were studying
mice to find the best way to make an AIDS vaccine. Their findings reveal that
the immune system, instead of being “blind” to HIV, can indeed produce cells
with the potential to combat the virus. However, these cells are killed off
before they can fully mature; apparently, they are viewed by the body as a
potential threat.

Just because these studies produced lackluster results,
however, doesn’t indicate that they aren’t meaningful. Even a failed experiment
can help guide future research; it tells scientists they need to try something
else. If they can take even a little information from the misstep to create a
better next experiment, then what appeared initially to be disappointment can
ultimately be viewed as a success.

Just look at the similarity between two statements on the
future of HIV research. Anthony Fauci, director of the National Institute of
Allergy and Infectious Diseases, said to the Post about the flawed study from September: “It does now form the
basis for … the development of future HIV vaccines.”

The senior author of the Duke study, Barton Haynes,
meanwhile, said the following: “This represents a new insight into the way HIV
effectively evades … and may offer new directions for vaccine design.”

There is hope that one day, one of these failures will lead
to a major breakthrough. In the meantime, we already have developed proven methods for preventing HIV. With enough awareness, the number of new infections
can be drastically reduced.

—Andrew Kahn

Flu may contribute to Parkinson’s, Alzheimer’s

Could the flu cause Parkinson’s or Alzheimer’s disease? The
answer may be yes, according to a new study by researchers at the University of
Tennessee, Memphis, and St. Jude’s Research Hospital. In particular, the
scientists found that the H5N1 flu strain—commonly known as bird flu—can
infiltrate deep into the brain, causing a “slow-burning” immune reaction that
may contribute to the onset of several neurodegenerative disorders.

The study, published
in Proceedings of the
National Academy of Sciences,
was inspired by reports that neurological
symptoms seemed to occur more frequently following the 1918 “Spanish flu.”
Similar signs appeared after recent cases of H5N1 in both people and animals.
So the scientists infected 225 mice with bird flu to study the virus’s effect
on the brain.

H5N1 is a
highly virulent strain of flu, and, as it does people who contract the disease,
it killed about half the mice. The other half showed signs of infection in
their brains, but within three weeks all active signs of flu infection—along
with any neurological symptoms—were gone. 
This recovery was only surface-deep, however: The researchers found that
the surviving mice had started to produce an abnormal, clumping form of a
protein known as alpha synuclein in their brains. Abnormal clumps of protein are
one of the hallmark
of Parkinson’s, Alzheimer’s and other neurodegenerative diseases.

In addition, signs of activated
microglia, the brain’s immune cells, indicated the presence of inflammation. These
factors were linked directly to brain cell death; within 60 days of infection, the
substantia nigra pars compacta regions of the mice brains showed a loss of
about one-fifth of their dopamine-producing neurons, a milder form of the
damage that occurs in Parkinson’s. The researchers also found aggregated
clusters of protein in the hippocampus, cortex and brainstem—as is often seen
in neurodegenerative diseases.

The researchers liken this to a
hit-and-run; they speculate that the flu virus causes the brain’s immune system
to turn on and then remain active long after the infection has been
eradicated.  If their theory holds, they
add, then any number of viruses that make their way past the brain’s defenses
could contribute to Alzheimer’s and Parkinson’s. (This also falls in line with
a popular theory about why some flu strains, particularly Spanish flu, become
so deadly and disproportionately kill off the young and healthy: They unleash a
an ultimately fatal overreaction by the immune system.)

For now, the findings are merely
informative. The study did not extend long enough to check whether full-blown
cases of Parkinson’s did occur in the mice, for instance, and more
research—especially in primates—is needed to confirm that the results translate
to humans. It’s also far too early to tell if bird flu survivors are
contracting these disorders more often. And even if verified, viral infections
are likely to just be another addition to the many risk factors, most notably
age, for such neurodegenerative disorders.

As for those worried about H1N1—the current
pandemic flu strain
—good news: It does not appear to attack the brain.

 —Aalok Mehta


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