Neurogenesis doesn’t fully stop. The production of new brain cells slows dramatically after early childhood, but the best available evidence shows that the human hippocampus continues generating roughly 700 new neurons per day well into adulthood, with a modest decline as you age. What makes this topic complicated is that scientists still disagree about exactly how much new neuron production persists, and where.
The Sharp Drop in Childhood
The vast majority of your brain’s neurons are produced before birth and during infancy. After that, the rate of new neuron creation falls off a cliff. Immunohistochemical studies of human brain tissue show a marked decline in neurogenesis in both of the brain’s known neuron-producing regions during early childhood. By adolescence, markers of cell division and immature neurons in these areas are a fraction of what they were in infancy.
This steep early decline is why some researchers have concluded that meaningful neurogenesis is essentially over by adulthood. A prominent 2018 study led by Shawn Sorrells examined brain tissue from subjects ranging from 14-week-old fetuses to 77-year-old adults and concluded that “human hippocampal neurogenesis drops sharply in children to undetectable levels in adults.” That paper made headlines and reignited a debate that had been simmering for years.
Evidence That It Continues
The most creative approach to settling this question came from a research team at the Karolinska Institute in Sweden. They took advantage of a grim relic of the Cold War: above-ground nuclear bomb tests conducted between 1955 and 1963, which released elevated levels of radioactive carbon-14 into the atmosphere. That carbon-14 was incorporated into the DNA of any cell dividing at the time. By measuring carbon-14 levels in hippocampal neurons from people aged 19 to 92, the researchers could determine when those neurons were born.
The results were striking. About one-third of hippocampal neurons turn over during a person’s lifetime. The annual turnover rate within that renewing population is 1.75%, translating to approximately 700 new neurons per hippocampus per day in adults. The decline with aging was modest. Perhaps most surprisingly, the rate of adult hippocampal neurogenesis in middle-aged humans was comparable to that in middle-aged mice, a species where adult neurogenesis is well established.
A separate 2018 study by Maura Boldrini’s team examined brain tissue from people aged 14 to 79 who had no psychiatric illness. They found that while some precursor cell populations and blood vessel growth declined with age, the number of immature neurons and mature new granule cells did not significantly decrease. Their conclusion: human hippocampal neurogenesis persists throughout aging.
Why Scientists Disagree
The contradiction between “neurogenesis stops in childhood” and “neurogenesis continues into old age” comes down partly to methodology. Identifying new neurons in human brain tissue is technically difficult. Researchers rely on proteins that mark dividing cells or immature neurons, but these markers can degrade after death, and how quickly tissue is preserved matters enormously. The Boldrini team has pointed out that the Sorrells study lacked detailed information about subjects’ psychiatric history, medications, and recent drug use, all of which can affect neurogenesis rates, particularly in the front portion of the hippocampus.
Another complicating factor: the sparse proliferating cells found in the adult brain are largely microglia (immune cells), not neuron precursors. Distinguishing between the two requires careful staining and analysis, and different labs use different techniques. Gene expression studies add another layer, showing that markers of cell proliferation and neuronal maturation decline significantly and progressively across the adult lifespan, even if they never reach absolute zero.
Where New Neurons Are Born
In adults, neurogenesis is restricted to two small zones. The first is the subgranular zone of the hippocampus, a structure deep in the brain that is critical for learning and memory. This is where the strongest evidence for ongoing human neurogenesis exists. Neural stem cells in this zone go through a multi-stage process: they first proliferate, then differentiate into intermediate progenitor cells, and finally mature into functional neurons.
The second zone is the subventricular zone, which lines the brain’s fluid-filled ventricles. In rodents and sheep, new neurons from this area migrate to the olfactory bulb and help process smell. In humans, this migration pattern appears to be different. Carbon-14 dating studies found no evidence of adult-born neurons reaching the human olfactory bulb. Instead, new cells from the subventricular zone appear to migrate into the nearby caudate nucleus, a region involved in movement and decision-making. This makes biological sense: smell is far less important to humans than to rodents, so the brain may have repurposed this neurogenic zone.
How Long New Neurons Take to Mature
When a new neuron is born in the hippocampus, it doesn’t become functional overnight. The entire maturation process takes roughly seven weeks. Within days of a stem cell’s final division, the new neuron extends an axon to its target area in the hippocampus and begins forming connections. For the first one to one and a half months, these young neurons go through a critical period of heightened flexibility, during which they show increased ability to strengthen or weaken their connections compared to older, established neurons. After about seven weeks, the new cells become essentially indistinguishable from their older neighbors.
This window of enhanced plasticity is thought to be part of why new neurons matter. They may be especially good at encoding new memories or distinguishing between similar experiences precisely because they’re still in this flexible, impressionable state.
What Slows Neurogenesis Down
Chronic stress is one of the most well-documented suppressors of new neuron production. When you’re stressed, your body releases cortisol, which easily crosses the blood-brain barrier and enters neurons. Cortisol binds to a specific receptor inside cells called the glucocorticoid receptor, and activation of this receptor directly inhibits the proliferation of neural progenitor cells. Animal studies from the early 1990s showed this clearly: administering stress hormones reduced new cell production, while removing the adrenal glands (which produce cortisol) boosted it.
The relationship is dose-dependent. Normal, fluctuating cortisol levels are part of healthy brain function and may actually help regulate neurogenesis so it doesn’t overshoot. The problem arises with chronically elevated cortisol, the kind associated with prolonged stress, sleep deprivation, or depression. Sustained high levels reduce not just the proliferation of new cells but also their differentiation and survival.
Age itself brings a progressive decline. Studies of human hippocampal tissue from people aged 18 to 88 show statistically significant decreases in gene expression for both cell proliferation markers and immature neuron markers across the lifespan. The decline is real, even if the process never fully stops.
What Supports New Neuron Growth
Aerobic exercise is the lifestyle factor most consistently linked to hippocampal health, though the evidence in humans is more nuanced than animal studies suggest. In rodents, running on a wheel reliably increases new neuron production. In humans, meta-analyses of randomized controlled trials have examined whether aerobic exercise training changes hippocampal volume in healthy older adults, but the results have been mixed, with no clear relationship between improvements in cardiovascular fitness and hippocampal volume changes. This doesn’t mean exercise has no effect on neurogenesis; it may mean that volume measurements are too crude to capture what’s happening at the cellular level.
Antidepressants, particularly those in the SSRI class, have been shown to increase hippocampal neurogenesis through an unexpected mechanism. Rather than acting independently, these medications appear to work by activating the same glucocorticoid receptor that stress hormones use to suppress neurogenesis. In laboratory studies, the antidepressant sertraline increased neuronal differentiation through this receptor, and it only boosted cell proliferation when cortisol or a cortisol-like compound was also present. This suggests antidepressants may work in part by changing how the brain responds to its own stress hormones, shifting the balance from suppression toward growth.
Neurogenesis and Brain Disease
Reduced neurogenesis appears to play a role in Alzheimer’s disease. Studies using single-cell genetic sequencing have confirmed that immature neurons exist in the adult human brain and that their numbers are reduced in people with Alzheimer’s. The genetic programs that normally drive neurogenesis in healthy adults are downregulated in both pre-clinical cognitive impairment and diagnosed Alzheimer’s disease. Whether this reduction is a cause or consequence of the disease remains an open question, but it fits with the broader understanding that the hippocampus is one of the first brain regions affected in Alzheimer’s and that memory formation, which new neurons support, is one of the earliest functions to decline.