There are certain parts of our brains that shrink by almost a third before age 65 due to normal aging. One of the things we’re trying to do through our brain aging initiative here is better understand this. There’s already good evidence there are certain things that we can do to promote neuroplasticity — the brain’s ability to be flexible and remodel itself in response to stimuli and insults.
Maintaining brain health through life is similar to maintaining heart health
First, we’re not designed to sit still. Research shows that increased exercise prompts the release of a hormone (brain drive neurotrophic factor) that repairs the brain at the molecular level. This can become particularly important as we age and we often quit exercising. We’ve published data showing that even modest exercise, like walking 10 to 20 minutes a day, can be sufficient to improve brain health.
There’s some evidence that what we eat changes the gut biome, and this also affects our brain in addition to any other vascular or metabolic damage from our diet. Either way, we’re not designed to eat fast-food hamburgers, and then take supplements to compensate. Taking fish oil if you’re eating processed beef is not going to help you. You have to fundamentally change your diet.
What we think is that we need to move to more fish (particularly fatty fish like salmon), and more vegetables, legumes and unprocessed grains. The so-called Mediterranean diet. The biggest problem — and another reason why brain health becomes a social issue — is that cost of food tends to rise.
Nearly as important as cardiovascular exercise is the idea of habitual exercise for the brain — developing a life of learning.
Trying new hobbies, learning languages, jumping into creative endeavors, engaging socially — these and similar new experiences have all been shown to have strong impacts on brain health.
What seems to be crucial is continued learning. It’s more than repeatedly playing a brain game or two until it becomes rote — it’s playing new games, putting your brain into a mode of learning that secretes the brain repair hormone. I like to say it’s when your head is hurting a little — you’re thinking things you haven’t before, making new connections. Even when you’re out of your comfort zone and you say, “Ugh, I hate this.” That’s when your brain is stretching. You’re not just punching the clock, so to speak.
What we think is that there’s a brain reserve, a cognitive reserve, which can be influenced or built up by the complexity of our activities. We do find that highly educated and accomplished people have less risk. When and if they get disease, the onset is delayed, and when it does appear the progression is steeper. The pathology exists but the brain is also more organized, so the person does well further into the disease, and then tends to decline precipitously at the end.
If you think of quality of life as an ability to engage in and enjoy life over a period of time, a steeper decline can actually reduce length of suffering — the theory of “compression of morbidity.”
Related UC Davis Research: Dementia-related brain damage begins in early middle age
UC Davis researchers have unearthed novel insights about the intersection of dementia and cardiovascular disease — including several drawing on the legendary Framingham Heart Study. Some highlights:
- A 2011 UC Davis-led analysis published in Neurology found that high blood pressure, diabetes, obesity and smoking in middle age can cause vascular damage, decreased brain volume and cognitive decline later in life. The study gave evidence “that identifying these risk factors early in middle age could be useful in screening people at risk of dementia, and in encouraging them to make lifestyle changes before it’s too late,” DeCarli said.
- A year later, another UC Davis-led analysis published in The Lancet Neurology was the first to demonstrate structural damage to the brains of adults in young middle age as a result of high blood pressure. The study found accelerated brain aging among hypertensive and prehypertensive people in their 40s — suggesting vascular brain injury “develops insidiously over the lifetime with discernible effects.”
- A 2013 UC Davis-led study published in JAMA Neurology enhanced the known relationship between high cholesterol and increased Alzheimer’s risk, becoming the first to specifically link higher cholesterol to deposits of amyloid plaque — a hallmark of Alzheimer’s — in living humans.
- The same year, a UC Davis study of diabetic dementia patients published in Annals of Neurology was the first to provide clear evidence that amylin, a protein secreted with insulin, accumulates in the same manner as amyloid plaques. “If we’re smart about treatment of pre-diabetes, a condition that promotes increased amylin secretion, we might be able to reduce risk of complications, including Alzheimer’s and dementia,” said co-author Florin Despa.
- A 2016 UC Davis-led study published in Stroke revealed for the first time that people as young as their 40s have stiffening of the arteries associated with brain damage implicated in cognitive decline and Alzheimer’s. As the earliest manifestation of systolic hypertension, arterial stiffness “may actually be a better measure of vascular health, and should be identified, treated and monitored throughout the lifespan,” said lead author Pauline Maillard.
- A UC Davis researcher leading the largest epidemiological study of women’s reproductive history and dementia shared results last year suggesting that reproductive events signaling different estrogen exposures may play a role in modulating dementia risk. Rachel Whitmer found correlations between dementia and number of children, number of miscarriages, age at first period, age at natural menopause, and total reproductive years.
- A first-of-its-kind UC Davis study published this spring in the Journal of Alzheimer’s Disease uncovered dramatic differences in the brains of Hispanics with a dementia diagnosis compared with non-Hispanic whites and African Americans. “If you are Latino and diabetic or black and hypertensive, you’re probably at higher risk for dementia and these risks should be addressed aggressively,” DeCarli said.