Yale University. US: Beta-amyloid is a sticky protein that aggregates and forms small
plaques in the brains of the elderly and is thought to be a cause of
Alzheimer’s disease. Because specialized immune cells always surround
these plaques, many have theorized that these cells are responsible for
inflammation and damage to surrounding brain cells.
That theory
appears to be wrong, according to a new study by Yale School of Medicine
researchers published in the Jan. 29 issue of Nature Communications.
Instead of causing damage, these brain immune cells — called microglia —
seem to protect the brain by keeping amyloid plaques corralled, the
paper shows.
Previous research had shown that some people with
large accumulations of plaques do not necessarily have symptoms of
dementia, which led researchers to search for other causes of cognitive
decline. Inflammation was one of potential culprits identified by
scientists. However Alzheimer’s drugs that target inflammation in the
brain have failed to show any benefit.
“The idea that inflammation
is always bad is a simplistic view and is probably wrong when talking
about Alzheimer’s,” said Jaime Grutzendler, associate professor in the
Department of Neurology and senior author of the study. “In fact, as we
age we lose microglia and become less able to confine plaques, leading
to the release of plaque toxins that destroy the connections between
neurons.”
The new study using high-resolution imaging technology
revealed that in the brains of mice, microglia actually act as a
physical barrier that slows the expansion of plaques and blocks the
ability of free-floating beta-amyloid proteins to bind to the plaques
and cause toxicity.
“One possibility is that microglia nicely
insulate the rest of the brain from plaques and may explain why some
people with them do not experience severe cognitive decline,”
Grutzendler said. “By improving microglia’s shielding function, we were
able to reduce toxicity to neurons.”
This insight could lead to new treatments for the disease, he added.
Carlo
Condello and Peng Yuan of Yale are co-first authors of the paper. The
research was funded by the National Institutes of Health.