Symptoms

formed next to plaques in mice with weak microglia than in those with functional immune cells, they reported in Nature Neuroscience.

Why? Normal microglia seem to restrict amyloid plaques, which limits damage to surrounding tissue — damage that can make it easier for tau to take hold, he explained.

While it was known that amyloid buildup drives tau tangles, “we never had a good clue as to how it is doing that,” Holtzman said. The new findings “would argue that these cells are sort of a missing link.”

Separately, biotech company Alector Inc. has begun first-step patient testing of a drug designed to boost TREM2 and better activate microglia. of infection with certain herpes strains.

And Cortexyme Inc. is enrolling more than 500 early-stage patients around the country to test a drug that targets potentially neuron-damaging substances produced by gingivitis bacteria.

Whether the germ theory is a worthwhile pursuit was hotly debated at an international Alzheimer’s Association meeting in July. One skeptic, Dr. Todd Golde of the University of Florida, cautioned that germs’ mere presence doesn’t mean they caused dementia — they could be a consequence of it.

Still, a 2018 study from Taiwan offered a hint that treating herpes infection might lower later dementia risk. And a U.S. study found certain herpes viruses affected the behavior of Alzheimer’s-related genes.

“Maybe these are just opportunistic pathogens that have space to spring up in the brains of people affected with Alzheimer’s disease,” said Benjamin Readhead of Arizona State University, who co-authored that U.S. paper. But, “it looks at least plausible that some of these pathogens are capable of acting as accelerants of disease.”

One key commonality among emerging Alzheimer’s theories is how aggressively the brain’s immune system defends itself — and thus how inflamed it becomes.

Remember how some people have lots of plaques and tangles but no dementia? A few years ago Massachusetts General researchers found strikingly little inflammation surrounded all the gunky buildup in the resilient brains — but the Alzheimer’s-affected brains harbored a lot.

Research since has found similar inflammatory effects with other forms of dementia.

A handful of drugs are being explored in the quest to tamp down inflammation’s damaging side without quashing its good effects. Take those microglia, which Holtzman said “may be a two-edged sword.”

Early on, before there’s too much plaque, revving them up may be good. But later on, a hyperactive swarm around growing plaques spews out inflammatory molecules.

In addition to their immune system job, microglia also secrete molecules that help nourish neurons, noted Kentucky’s Wilcock. The goal is to restore the natural balance of a healthy brain’s environment, she said, so microglia “can perform their essential functions without damaging surrounding tissue.”

All those drug flops weren’t a waste of time.

“Every time there’s a failure it’s absolutely clear that we learn a lot,” Emory University neurologist Dr. Allan Levey recently told the government’s Alzheimer’s advisory council.

One lesson: Timing may matter. Most of the failed anti-amyloid drugs were tested in people who already had at least mild symptoms. Some studies seeking to prevent memory loss in the first place still are underway. Anti-tau drugs also are being tested.

Another lesson: Most people have a mix of different dementias, which means they’ll need a variety of treatments.

“Now we have an opportunity, a real opportunity, to expand and try all these avenues,” said Alzheimer’s Association chief science officer Maria Carrillo. “The triggers as we understand them are broad.”

All too often, easy-toread signs indicating where patients should go can’t be found.

Last year, a committee examining how Long Island Jewish Medical Center should handle patients with special needs (for instance, people with cognitive impairments or hearing or speech problems) identified better signage as a priority.

Now, signs in the parking lot and outside the medical center are bigger, with larger type.

Inside the medical center, large signs have been placed at bathrooms, showing clearly if they’re accessible to those with disabilities. And the staff is creating a comprehensive map of the hospital campus — a handout.

At Northwestern, Lindquist realized that older patients were having trouble seeing whiteboards in their hospital rooms listing scheduled procedures and the names of physicians and nurses responsible for their care. Upon Lindquist’s urging, the hospital bought whiteboards that are more than double the normal size.

At a recent talk in the San Francisco Bay Area to promote her new book, “Elderhood,” Dr. Louise Aronson was approached by an older woman who uses a portable oxygen tank to breathe and relies on a rollator walker (with a seat and basket attached).

The woman was new to the area and had been visiting various medical facilities. “Some of these places have ramps, but

Ashkenaz has another pet peeve: chairs in waiting rooms with seats that are too low or without arms that she can grab to push herself up into a standing position.

At her cardiologist’s office, there’s a sofa with deep seats. “It looks nice, but I’d do anything not to sit there,” Ashkenaz said. “I just can’t get up from it.”

Wei’s clinic at the University of Arkansas has brought in chairs that are 4 inches taller than usual, with arms, for older patients. “These chairs are always occupied,” she said.

Also, exam rooms at the clinic are large enough to accommodate chairs for multiple family members. “We’ll bring everyone in to talk about mom or dad so they can hear what the other person is saying,” Wei said.