The protein responsible for forming plaques in the brains of people with Alzheimer’s disease could double as an microbe-fighting agent, according to research published last week in the journal PLoS One.
The protein, called amyloid-beta, aggregates into toxic plaques that destroy signals between neurons, causing Alzheimer’s sufferers to lose their memories. Long thought as simply a waste product of the brain, the new study suggests that the material has protective benefits, too.
“For years we thought that [amyloid]-beta was just metabolic garbage produced as a byproduct of other processes within the brain,” said study author Rudolph Tanzi, a neurologist at the Massachusetts General Institute for Neurodegenerative Disease in Boston, in a press release. “But these data suggest it is a normal component of the brain’s innate immune system.”
The study was triggered by a curious observation between Tanzi and his colleague Robert Moir: They noticed an uncanny likeness between amyloid-beta and an antimicrobial peptides called cathelicidin, also known as LL-37. The researchers then tested the amyloid proteins against 12 bacteria that LL-37 is known to kill, and found that amyloid-beta could kill eight of the microbial species, which are known to infect a range of tissues, including the central nervous system. Brain samples from Alzheimer’s patients also had more potent killing power than samples from healthy brains.
Not all Alzheimer’s researchers are convinced that amyloid-beta is truly part of the innate immune system, however. Norman Relkin, a neurologist at the New York Presbyterian Hospital–Weill Cornell Medical Center hospital, told the New York Times that the idea was “unquestionably fascinating,” but cautioned that the evidence for it was “a bit tenuous.”
The findings add to the list of cell types that can be damaged by amyloid-beta, including neurons, glia and epithelial cells.
What do you think? Could amyloid-beta be a bacterial-killer in the brain gone astray? Please leave a comment below.
Image: Amyloid-beta transmembrane structure via Wikimedia Commons
