Until recently, it was believed the human brain contained all the neurons it would ever have at the time of birth. And while it’s true that most of our brain cells are developed when we’re very young, there is some evidence to suggest that our bodies continue to develop these cells not only into adulthood but also into old age. In people with Alzheimer’s disease, however, the production of new neurons trails off, leading researchers to believe that developing a way to promote the creation of new neurons could protect people from dementia.
In an effort to find out how long neurogenesis—the process of creating new neurons—extends in humans, researchers studied the brains of 13 deceased people. These people ranged from 43 to 87 years old and died of different causes, such as cancer, stroke, and sepsis, but their brains were all considered healthy.
The team was particularly interested in looking at the dentate gyrus region of the hippocampus to see if there were signs of immature neurons being formed. And indeed, they did find that all their specimens still had new neurons, called doublecortin-expressing (DCX+) neurons, growing in their brains, even the 87-year-old specimen. This leads researchers to conclude that we can form new neurons and new neuronal connections throughout our entire life, keeping our brains healthy.
“Our research group is focused on investigating the mechanisms that control adult hippocampal neurogenesis, both under physiological and pathological conditions,” the team’s lab website explains. “In particular, we are interested in determining the therapeutic potential of increasing adult hippocampal neurogenesis for the treatment of neurodegenerative diseases such as Alzheimer’s disease (AD) and other tauopathies.”
Unlike in people with healthy brains, in people with Alzheimer’s, the generation of new neurons trails off and stops completely, leaving the remaining neurons to wither and die over time, taking the patients’ memories and skills with them. The team studied 45 brains of deceased Alzheimer’s patients between the ages of 52 and 97 and found “a marked and progressive decline in this number as the disease advanced.”
“The number of DCX+ cells detected in neurologically healthy individuals of any age was consistently higher than that found in patients with AD, regardless of the age of these patients,” say the researchers. “These data strongly support the notion that AD is a condition that differs from physiological aging and suggest that, despite a physiological age-related decline in the population of DCX+ cells, independent neuropathological mechanisms contribute to devastating the population of immature neurons in AD.”
Researchers hope that their new understanding of neurogenesis will aid in the future development of prevention and treatment methods for Alzheimer’s disease. Interestingly, they also noted during the study that the decrease in generation of new neurons in patients with Alzheimer’s began to happen before other changes were very noticeable in the brain, such as the neurofibrillary tangles and plaques normally associated with the disease. This could shed new light on our efforts to diagnose the disease early using noninvasive methods capable of picking up on biomarkers like decreased neurogenesis.
There is a lot of research yet to be done before any of this information can be truly helpful to Alzheimer’s patients, and that includes research on living patients, but we are grateful as usual for another step in the right direction and another avenue opened up for further research. For now, the best protection against the disease seems to be to continue forcing our brains to stay active and learn new things.
“I believe we would be generating new neurons as long as we need to learn new things,” says researcher Dr. Maria Llorens-Martin. “And that occurs during every single second of our life.”
Elizabeth Nelson is a wordsmith, an alumna of Aquinas College in Grand Rapids, a four-leaf-clover finder, and a grammar connoisseur. She has lived in west Michigan since age four but loves to travel to new (and old) places. In her free time, she. . . wait, what’s free time?