With apologies for length, here is information that might
interest anyone concerned about "cognitive deficits" for themselves
or loved ones.
Plant Flavonoid In Celery And Green Peppers Found To Reduce
Inflammatory Response In The Brain
A plant compound found in abundance in celery and green peppers can
disrupt a key component of the inflammatory response in the brain.
ScienceDaily (May 23, 2008) Researchers at the University of
Illinois report that a plant compound found in abundance in celery and
green peppers can disrupt a key component of the inflammatory response
in the brain. The findings have implications for research on aging and
diseases such as Alzheimer's and multiple sclerosis.
Inflammation can be a blessing or a blight. It is a critical part of
the body's immune response that in normal circumstances reduces injury
and promotes healing. When it goes awry, however, the inflammatory
response can lead to serious physical and mental problems.
Inflammation plays a key role in many neurodegenerative diseases and
also is implicated in the cognitive and behavioral impairments seen in
The new study looked at luteolin (LOO-tee-OH-lin), a plant flavonoid
known to impede the inflammatory response in several types of cells
outside the central nervous system. The purpose of the study was to
determine if luteolin could also reduce inflammation the brain, said
animal sciences professor and principal investigator Rodney Johnson.
"One of the questions we were interested in is whether something like
luteolin, or other bioactive food components, can be used to mitigate
age-associated inflammation and therefore improve cognitive function
and avoid some of the cognitive deficits that occur in aging," Johnson
The researchers first studied the effect of luteolin on microglia.
These brain cells are a key component of the immune defense. When
infection occurs anywhere in the body, microglia respond by producing
inflammatory cytokines, chemical messengers that act in the brain to
orchestrate a whole-body response that helps fight the invading
This response is associated with many of the most obvious symptoms of
illness: sleepiness, loss of appetite, fever and lethargy, and
sometimes a temporary diminishment of learning and memory.
Neuroinflammation can also lead some neurons to self-destruct, with
potentially disastrous consequences if it goes too far.
Graduate research assistant Saebyeol Jang studied the inflammatory
response in microglial cells. She spurred inflammation by exposing the
cells to lipopolysaccharide (LPS), a component of the cell wall of
many common bacteria.
Those cells that were also exposed to luteolin showed a significantly
diminished inflammatory response. Jang showed that luteolin was
shutting down production of a key cytokine in the inflammatory
pathway, interleukin-6 (IL-6). The effects of luteolin exposure were
dramatic, resulting in as much as a 90 percent drop in IL-6 production
in the LPS-treated cells.
"This was just about as potent an inhibition as anything we had seen
previously," Johnson said.
But how was luteolin inhibiting production of IL-6?
Jang began by looking at a class of proteins involved in intracellular
signaling, called transcription factors, which bind to specific
"promoter" regions on DNA and increase their transcription into RNA
and translation into proteins.
Using electromobility shift assays, which measure the binding of
transcription factors to DNA promoters, Jang eventually determined
that luteolin inhibited IL-6 production by preventing activator
protein-1 (AP-1) from binding the IL-6 promoter.
AP-1 is in turn activated by JNK, an upstream protein kinase. Jang
found that luteolin inhibited JNK phosphorylation in microglial cell
culture. The failure of the JNK to activate the AP-1 transcription
factor prevented it from binding to the promoter region on the IL-6
gene and transcription came to a halt.
To see if luteolin might have a similar effect in vivo, the
researchers gave mice luteolin-laced drinking water for 21 days before
injecting the mice with LPS.
Those mice that were fed luteolin had significantly lower levels of
IL-6 in their blood plasma four hours after injection with the LPS.
Luteolin also decreased LPS-induced transcription of IL-6 in the
hippocampus, a brain region that is critical to spatial learning and
The findings indicate a possible role for luteolin or other bioactive
compounds in treating neuroinflammation, Johnson said.
"It might be possible to use flavonoids to inhibit JNK and mitigate
inflammatory reactions in the brain," he said. "Inflammatory cytokines
such as interleukin-6 are very well known to inhibit certain types of
learning and memory that are under the control of the hippocampus, and
the hippocampus is also very vulnerable to the insults of aging," he
said. "If you had the potential to decrease the production of
inflammatory cytokines in the brain you could potentially limit the
cognitive deficits that result."
The study appeared recently in Proceedings of the National Academy of
Adapted from materials provided by University of Illinois at