(AP) — When researchers at the University of Kentucky compare brains donated from people who died with dementia, very rarely do they find one that bears only Alzheimer’s trademark plaques and tangles — no other damage.
If they do, “we call it a unicorn,” said Donna Wilcock, an Alzheimer’s specialist at the university’s aging center. Contrary to popular perception, “there are a lot of changes that happen in the aging brain that lead to dementia in addition to plaques and tangles.”
That hard-won lesson helps explain how scientists are rethinking Alzheimer’s.
For years researchers have been guided by one leading theory — that getting rid of a buildup of a sticky protein called amyloid would ease the mind-robbing disease. Yet drug after drug has failed. They might clear out the gunk, but they’re not stopping Alzheimer’s inevitable worsening.
The new mantra: diversify.
With more money — the government had a record $2.4 billion to spend on Alzheimer’s research this year — the focus has shifted to exploring multiple novel ways of attacking a disease now considered too complex for a one-size-fits-all solution. On the list, researchers are targeting the brain’s specialized immune system, fighting inflammation, even asking if simmering infections play a role.
Some even are looking beyond drugs, testing if electrical zaps in the brain, along a corridor of neural connections, might activate it in ways that slow Alzheimer’s damage. Tuesday, doctors at Barrow Neurological Institute in Phoenix announced they had implanted a pacemaker-like “deep brain stimulation” device into the first of more than 200 patients for an international study .
Most of the fresh starts for drugs are in the earliest research stages. It’s far from clear that any will pan out, but “the field is now much more open-minded than it ever was to alternative ideas,” Wilcock said.
BREAKING THE PLAQUE AND TANGLE LINK
No one knows what causes Alzheimer’s but amyloid deposits were an obvious first suspect, easy to spot when examining brain tissue. But it turns out that gunk starts silently building up 20 years before any memory loss, and by itself it’s not enough to cause degeneration.
Sometime after plaques appear, another protein named tau starts forming tangles inside neurons, heralding cell death and memory loss.
But again, not always: Autopsies show sometimes people die with large amounts of both plaques and tangles, yet escape dementia.
So something else — maybe several other things — also must play a role. One possible culprit: The brain’s unique immune cells, called microglia (my-kroh-GLEE’-ah).
No surprise if you’ve never heard of microglia. Neurons are the brain’s rock stars, the nerve cells that work together to transmit information like memories. Microglia are part of a different family of cells long regarded as the neurons’ support staff. But “it’s becoming clear they’re much more active and play a much more significant role,” said Dr. Richard Hodes, director of the National Institute on Aging.