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After about age 40, our brains begin to lose a step or two.

Each year, our reaction time slows by a few thousandths of a second. We’re also less able to recall items on a shopping list.

Those changes can be signs of a disease, like Alzheimer’s. But usually, they’re not.

“Both of those things, memory and processing speed, change with age in a normal group of people,” says Matt Huentelman, a professor at TGen, the Translational Genomics Research Institute, in Phoenix.

Huentelman should know. He helps run MindCrowd, a free online cognitive test that has been taken by more than 700,000 adults.

About a thousand of those people had test scores indicating that their brain was “exceptional,” meaning they performed like a person 30 years younger on tests of memory and processing speed.

Genetics played a role, of course. But Huentelman and a team of researchers have been focusing on other differences.

“We want to study these exceptional performers because we think they can tell us what the rest of us should be doing,” he says.

Early results suggest that sleep and maintaining cardiovascular health are a good start. Other measures include avoiding smoking, limiting alcohol and getting plenty of exercise.

Huentelman was one of several dozen researchers who met in Miami this summer to discuss healthy brain aging. The event was hosted by the McKnight Brain Research Foundation, which funds studies on age-related cognitive decline and memory loss.

To preserve cognitive function in later life, “we’re going to have to understand [brain] aging at a mechanistic level,” says Alice Luo Clayton, a neuroscientist who is the group’s chief executive officer.

Another speaker was Christian Agudelo, a sleep neurologist at the University of Miami’s Evelyn F. McKnight Brain Institute.

“I think the value of sleep and sleep deprivation became true to me when I had kids,” Agudelo says.

Those kids are 4 and 6 now, so Agudelo is getting more sleep. But his own experience is consistent with his research on the relationship between sleep and cognitive decline.

“The better you sleep, the better your brain health is going to be both structurally and functionally,” Agudelo says.

Keep in mind: Better sleep isn’t just about getting more sleep.

The key is getting high-quality sleep, which allows the brain to cycle through all the sleep stages, Agudelo says.

Researchers can measure how well a person is sleeping by monitoring their brain wave patterns. But people usually know when they’ve had a good night’s rest, Agudelo says.

“You go to sleep, you wake up and you feel like that experience was worthwhile,” he says. “You feel refreshed.”

Ensuring high-quality sleep is tricky. But people can improve the odds with certain behaviors, Agudelo says

“Waking up at the same time every single day and aligning our sleep rhythms with the rhythm of the sun” can lead to better sleep, he says. So can “being active, both socially and physically.”

Those behaviors increase “sleep pressure,” the body’s natural desire to sleep the longer we are awake, Agudelo says. When that pressure is high, he says, “we can fall asleep more easily and deeply.”

Brain aging is also influenced by vascular risk factors, like blood pressure, cholesterol levels and diabetes, says Charles DeCarli, a neurologist who co-directs the Alzheimer’s Disease Research Center at the University of California, Davis.

People know that these risk factors usually contribute to medical conditions like heart attack or stroke, DeCarli says. But research on thousands of people 65 and older has found that these risk factors can also impact the brain directly — even if they don’t cause a heart attack or other cardiovascular problems.

“The size of the brain, the shape of the brain, the tissue integrity of the brain looks older in people who have these risk factors than in people who do not have them,” he says.

So DeCarli and a team of researchers are studying whether it’s possible to protect the brain by aggressively treating conditions that affect the circulatory system.

“The question is, if you have these diseases and they are well controlled, will you have a younger-looking brain?” he says. “And the answer seems to be yes.”

The patient: A 38-year-old woman in New Delhi

The symptoms: The patient had given birth via emergency cesarean section in another country, and after the operation, she noted pain on the right side of her lower abdomen. Doctors at the time told her it was normal postoperative pain, and they didn’t explore it further. Eventually, a lump formed at the site, and the woman’s pain intensified.

Catheter ablation procedures involving transseptal puncture — typically used to treat atrial fibrillation — are often linked to migraine-like visual auras, though the underlying cause has been unclear.

New evidence suggests these auras may stem not from the puncture itself but from acute, procedure-related brain emboli affecting the visual cortex.

“These research findings have two distinct clinically relevant implications,” senior author Gregory Marcus, MD, MAS, cardiac electrophysiologist and endowed professor of atrial fibrillation research, University of California San Francisco (UCSF), told Medscape Medical News.

“First, they suggest that migraine symptoms with visual auras are less likely to be due to shunting of some neuroactive compound across interatrial septal defects and more likely occur as a result of occlusion of blood flow due to brain emboli,” Marcus said.

“Second, these findings demonstrate that, contrary to a long-held belief that these post-ablation MRI-detected small brain lesions are asymptomatic — in fact, they are often referred to as ‘asymptomatic cerebral emboli’ or ‘ACEs’ — these small acute brain lesions actually can, and perhaps often do, manifest in clinical symptoms,” he added.

“This finding could change the whole paradigm of treatment, perhaps focusing more on prevention of blood clots,” he added in a statement.

The study was published online on July 7 in the journal Heart Rhythm.

Brain Injury From Catheter Ablation?

The TRAVERSE trial enrolled 146 adults undergoing catheter ablation for ventricular arrhythmias; 74 were randomly allocated to ventricular access via transeptal puncture (creating a new, temporary hole between the left and right atria) and 72 to a retrograde approach (through the aortic valve, not requiring transseptal puncture).

All patients underwent high-resolution brain MRI the day after ablation and 63 (85%) in the transseptal group and 57 (79%) in the retrograde group completed a validated migraine questionnaire, a median of 38 days after the procedure.

There was no difference in post-ablation visual auras between the transseptal and retrograde aortic approaches (16% and 14%, respectively).

However, significantly more patients with acute brain emboli in the occipital or parietal lobes reported migraine-related visual auras (38% vs 11%; P < .01).

After multivariable adjustment, the presence of acute brain emboli in the occipital or parietal lobes was associated with a 12-fold greater likelihood of visual auras.

The data show that these post-ablation brain lesions are not “clinically silent,” first author Adi Elias, MD, cardiac electrophysiology fellow at UCSF, noted in the statement. “It may be the case that we haven’t known what to look for and assessed for symptoms immediately without enough time for the subsequent visual auras that would occur,” Elias said.

Marcus elaborated on this point. He noted that prior studies have demonstrated that these small post-catheter ablation MRI-detected lesions can no longer be detected upon repeat imaging about a month later, demonstrating that the ability to detect these brain emboli is fleeting.

“Prior studies failed to demonstrate a relationship between migraine with visual aura and acute brain emboli, but perhaps they were too late to detect ephemeral MRI findings because the MRI had to be ordered and performed after symptoms develop,” Marcus said.

The TRAVERSE study is “unique in that everyone had a brain MRI immediately after their catheter ablation procedure and likely in most, if not all cases, prior to the development of their visual aura symptoms,” he noted.

Importantly, said the researchers, the presence of brain emboli and visual auras was not associated with any significant change in cognition. Marcus said patients can be reassured that procedure-related brain emboli and visual auras typically fade within a month of the procedure.

An Under-Recognized Condition

Reached for comment, Mina Chung, MD, president of the Heart Rhythm Society, who wasn’t involved in the study, told Medscape Medical News the occurrence of visual auras after ablation may be “under-recognized.”

The fact that a prior history of visual auras was associated with visual auras at 1 month after the procedure, “suggests some preexisting tendency toward such symptoms after these procedures,” said Chung, with the Department of Cardiovascular Medicine, Heart, Vascular, and Thoracic Institute, Cleveland Clinic, Cleveland.

“Reassuringly, there were no detectable differences in neurocognitive function,” said Chung.

This trial was funded by a grant from the Patient Centered Outcomes Research Institute (PCORI). Marcus is a consultant for and owns equity in InCarda and receives research funding from the National Institutes of Health and PCORI. Chung had no relevant disclosures.