Brain blood flow finding gives hope for Alzheimer’s therapy

You know that dizzy feeling you get when, after lying down for an extended period, you stand up a little too quickly?

That feeling is caused by a sudden reduction of blood flow to the brain, a reduction of around 30 percent. Now imagine living every minute of every day with that level of decreased blood flow.

People with Alzheimer’s disease don’t have to imagine it. The existence of cerebral blood flow reduction in Alzheimer’s patients has been known for decades, but the exact correlation to impaired cognitive function is less understood.

“People probably adapt to the decreased blood flow, so that they don’t feel dizzy all of the time, but there’s clear evidence that it impacts cognitive function,” said an associate professor.

A new study  offers an explanation for this dramatic blood flow decrease: white blood cells stuck to the inside of capillaries, the smallest blood vessels in the brain. And while only a small percentage of capillaries experience this blockage, each stalled vessel leads to decreased blood flow in multiple downstream vessels, magnifying the impact on overall brain blood flow.

The paper’s co-lead authors said, the study is the culmination of approximately a decade of study, data gathering and analysis. It began with a study in which one of the author was attempting to put clots into the vasculatures of Alzheimer’s mouse brains to see their effect.

“It turns out that … the blockages we were trying to induce were already in there,” she said. “It sort of turned the research around – this is a phenomenon that was already happening.”

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The researchers, determined that only about 2 percent of brain capillaries had “stalls” (blockages), but the cumulative effect of that small number of stalls was an approximately 20 percent overall decrease in brain blood flow, due to the slowing of downstream vessels by the capillaries that were stalled. Recent studies suggest that brain blood flow deficits are one of the earliest detectable symptoms of dementia.

To test the effect of the stalls on performance of memory tasks in Alzheimer’s mice, they were given an antibody that interfered with the adhesion of white blood cells to capillary walls, which caused the stalled capillaries to start flowing again and thus increased overall brain blood flow. Memory function was improved within a few hours, even in aged mice with more advanced stages of Alzheimer’s disease.

The authors are quick to point out, however, that the antibody is not something that can be used in humans. Also, of course, interfering with white blood cell adhesion would render an individual immunocompromised.

“What we’ve done is identify the cellular mechanism that causes reduced brain blood flow in Alzheimer’s disease models, which is neutrophils [white blood cells] sticking in capillaries,” the author said. “We’ve shown that when we block the cellular mechanism [that causes the stalls], we get an improved blood flow, and associated with that improved blood flow is immediate restoration of cognitive performance of spatial- and working-memory tasks.”

“Now that we know the cellular mechanism,” he said, “it’s a much narrower path to identify the drug or the therapeutic approach to treat it.”

The team has identified approximately 20 drugs, many of them already government approved for human use, that have potential in dementia therapy. Some of them, however, were designed to be taken in high doses for short periods of time to treat sepsis, or in the immediate aftermath of a heart attack or stroke. “They weren’t really intended to be something that you take for the rest of your life,” the author said. Nonetheless, the lab is screening these drugs in Alzheimer’s mice now. 

The author said he’s “super-optimistic” that, if the same capillary-blocking mechanism is at play in humans as it is in mice, this line of research “could be a complete game-changer for people with Alzheimer’s disease.”