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Washington – 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.

No one knows what causes Alzheimer’s but amyloid deposits were an obvious first suspect.

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