93 people with an average age of 60 learned to juggle. Their brains grew. Then they stopped juggling, and their brains went back.
The word "neuroplasticity" has been doing promotional work for about fifteen years. It shows up in app store copy, in supplement marketing, and in the sentence "your brain can rewire itself at any age", which is true in the same loose way that "your body can build muscle at any age" is true, and just as unhelpful on its own.
The interesting question isn't whether the aging brain can change. It can. The question is what kind of change, how much, how long it lasts, and whether any of it shows up in a life rather than a scanner.
Why This Matters
If plasticity is a capacity that fades on a schedule, then the sensible response is acceptance and a good hearing aid. If it's a capacity that responds to load and decays without it, the response is completely different: it's maintenance, indefinitely, with no finish line.
The evidence points at the second one. That's a harder message than the marketing version, because it means the effects you buy are rented, not owned. It also means a decent chunk of what gets sold as brain health is measuring the wrong thing.
This sits next to what we know about keeping the brain adaptable and the environmental exposures that shape brain aging. Here I want to be narrower: what does the plasticity research actually measure, and what does it support?
How To Read The Numbers Below
Four ideas will make the rest of this readable.
A standard deviation, written SD, is a unit of spread. When a cognitive result is reported as "0.24 SD per year", it means the group moved about a quarter of the typical spread between people, each year. Small effects on cognitive tests usually sit under 0.2 SD.
The bracketed range after a number is the set of values compatible with the data. If it includes zero for a difference, or 1.0 for a ratio, then "no effect" is still one of the values that fits.
"No significant effect" is not "no effect." It often means the study was too small to see one. Where that matters below, the number of participants is given so you can judge how much could be hiding in a null result.
Gray matter volume is a proxy, not a headcount. MRI voxel-based morphometry detects a change in signal density in a region. What cells or processes produce that change is still an open question. Treat every volume result in this article as a signal that something happened, not as a count of neurons.
Four Different Things Wearing One Name
"Neuroplasticity" collapses at least four separate biological processes, and they age differently.
Synaptic strength. Existing connections get stronger or weaker with use. This is the fastest form of change, operating in minutes to hours, and it's what underlies ordinary learning.
Structural change. Dendrites branch, spines appear and retract, and regions change measurable volume over weeks to months.
Myelin plasticity. The insulation on axons thickens with practice, which changes conduction speed. This one is the newest to human research and the least well characterised in older adults.
Neurogenesis. Genuinely new neurons, born from progenitor cells. In adult humans this is confined, if it happens at all, to the hippocampus, and it has been the subject of a long fight.
Most popular writing about brain plasticity quietly borrows the drama of the fourth to describe the first. They are not the same claim and they don't carry the same evidence.
The Thing That Declines, and One Thing That Apparently Doesn't
Start with what shrinks. In 142 healthy adults aged 60 to 91, followed with repeated MRI over a single year, cortical thinning was measurable after twelve months, running at roughly 0.5 percent a year in temporal and prefrontal cortex [1]. Nearly every subcortical region changed significantly over that year too. This is healthy aging, not disease.
So the obvious inference is that synapses are disappearing along with the tissue. That inference has now been tested directly, and it did not hold up cleanly.
Researchers scanned 80 healthy volunteers spanning seven adult decades with a PET tracer that binds SV2A, a protein found in presynaptic terminals, which serves as a living proxy for synaptic density [2]. After correcting for the tissue shrinkage described above, they found no significant cortical decline in synaptic density with age. The one clear age effect was in the caudate nucleus, at about 1.7 percent per decade. The hippocampus showed a 2 percent per decade reduction that did not reach significance.
That result deserves to be held loosely, since other groups using different correction methods have reported broader declines. But it's a useful corrective. The healthy older brain is smaller. The evidence that its remaining tissue is less densely connected is weaker than most people assume.
The Neurogenesis Fight, and Why It Took Seven Years
In March and April of 2018, two papers landed weeks apart with opposite conclusions.
Sorrells and colleagues examined hippocampal tissue from 59 people in Nature and reported that markers of young neurons dropped sharply through childhood and were undetectable in anyone over 13 [3]. Boldrini and colleagues examined tissue from 28 people aged 14 to 79 in Cell Stem Cell and reported that neurogenesis persists throughout aging, with large variation between individuals [4].
Both used postmortem human tissue. Both were careful. The disagreement came down substantially to technical detail: how long tissue sat before fixation, which antibodies were used, and how a "young neuron" was defined. A 2019 Nature Medicine paper from Moreno-Jiménez and colleagues, which controlled tissue handling tightly, found thousands of immature neurons per cubic millimetre in neurologically healthy people aged 43 to 87, dropping sharply in Alzheimer's disease [5].
The most direct evidence arrived in July 2025. Using single nucleus RNA sequencing and machine learning on hippocampal tissue, a group at Karolinska identified actively dividing neural progenitor cells in adults, including donors in their late seventies [6]. That's a different kind of evidence than a stain: it's a transcriptional signature of cells caught in the act.
Current reading: adult human hippocampal neurogenesis appears real, is highly variable between people, and is small. Nobody has shown that it can be raised deliberately in a human, or that raising it would change anything you'd notice. Treat any product claiming to boost it as marketing.
The Jugglers
Here's the study I keep coming back to.
In 2004, Draganski and colleagues taught young adults a three-ball cascade over three months and found gray matter increases in mid-temporal visual areas and the left posterior intraparietal sulcus [7]. Then they stopped the training. The increases faded.
In 2008, the same group ran it in older people: 93 healthy volunteers with a mean age of 60 [8]. They learned to juggle, less proficiently than 20-year-olds, but they learned. Gray matter increased in area hMT/V5, in the left hippocampus, and in the nucleus accumbens bilaterally. Three months after training ended, those changes had reversed.
Two things sit inside that result, and the second one gets ignored.
First, the aging brain restructures itself in response to a new skill. That's the encouraging half, and it's the half that gets quoted.
Second, the restructuring is contingent on continued use. The brain didn't bank the gain. It maintained a structure while the structure was being used and released it when it wasn't. Compare this with what happens to London taxi drivers, who spend three to four years learning 25,000 streets: those who qualified showed increased posterior hippocampal gray matter, and those who trained but failed did not [9]. That's a demanding, sustained load producing a change tied to actually succeeding.
Plasticity, on this evidence, behaves less like a savings account and more like aerobic fitness. You hold it by continuing to pay for it.
The Aging Brain Doesn't Just Do Less, It Does Different
One of the more durable findings in cognitive neuroscience is that older adults performing the same task as younger adults use more brain, not less.
Cabeza described this as hemispheric asymmetry reduction: prefrontal activity that's one-sided in young adults becomes bilateral in older adults, and the ones who recruit both sides tend to perform better, not worse [10]. Reuter-Lorenz and Park folded this into scaffolding theory, which frames the extra recruitment as compensation built in response to structural decline [11].
This reframes what "keeping your brain young" would even mean. An older brain that performs well is often not doing the young thing more efficiently. It's doing a different thing that works. Research suggests the scaffolding itself is built by engagement, novelty and challenge, which is a mechanism for why cognitive reserve behaves the way it does.
What Actually Moves the Numbers
Now the practical part, in descending order of evidence quality.
Aerobic exercise: real, and smaller than advertised. The famous result is Erickson's 2011 trial, where a year of walking increased anterior hippocampal volume by about 2 percent in older adults while the control group declined [12]. That study is still cited as though it settled the matter. It didn't. A meta-analysis of 14 randomised trials and 737 participants found no significant effect of aerobic exercise on total hippocampal volume [13]. What did survive was a significant effect on left hippocampal volume, and post hoc analysis indicated the mechanism was prevention of the decline that happens over time, rather than growth. So the honest framing is preservation. That's still worth having, and it's not what "exercise grows your brain" implies. Zone 2 work remains the most evidenced input here.
Cognitive training: durable, and narrow. The ACTIVE trial randomised 2,832 older adults to ten sessions of memory, reasoning or speed training [14]. Ten years later, the reasoning and speed groups still outperformed controls on reasoning and speed. The memory group did not hold its gain. Self-reported daily function held up better in all three trained groups: at a mean age of 82, about 60 percent of trained participants were at or above their baseline function versus 50 percent of controls. That's a real result from a large trial. It is also the ceiling of what commercial brain training has demonstrated, and a large consensus review concluded that evidence for transfer to untrained abilities or everyday performance is thin [15]. You get better at what you train.
Hearing: the strongest single lever in the risk-factor list. In ACHIEVE, three years of hearing intervention did not slow cognitive decline in the overall sample of 977 people [16]. In the prespecified subgroup at higher risk, drawn from the ARIC cohort, decline was 48 percent slower. That's a subgroup finding and should be read as such. But hearing loss is the largest single modifiable dementia risk factor in the 2024 Lancet Commission's accounting of 14 factors covering roughly 45 percent of cases [17], and the intervention is cheap and reversible.
Multidomain programmes: modest, and now tested at scale in the US. US POINTER randomised 2,111 older adults at risk of decline to a structured or self-guided lifestyle programme [18]. Both improved. The structured arm improved faster, at 0.243 SD per year versus 0.213. That gap is small. What the trial can't tell you is how much either arm beats doing nothing, because there was no such group.
What This Changes on a Tuesday
Four things follow from the evidence above, and they're less exciting than the field's press coverage.
Get your hearing tested if you're over 60. It's the cheapest intervention with a plausible mechanism and a randomised trial behind it.
Pick a skill that's genuinely hard and keep doing it. The juggling result says the structural change tracks ongoing practice. An instrument, a language, a sport with a motor learning component. Not an app that trains the same task you'll be tested on.
Treat exercise as preservation of brain tissue rather than growth of it, and do it anyway. The meta-analytic effect is on holding the left hippocampus, which is a slower-decline story, and slower decline compounds.
Stop paying attention to whether something "boosts neuroplasticity". No supplement has been shown to do this in a way that changes a human outcome, and the phrase is used almost entirely by people selling something.
The unglamorous inputs still dominate: sleep, blood pressure, social contact, and hearing. None of them are new. All of them are better evidenced than anything with "neuro" in the product name.
Frequently Asked Questions
Can adults really grow new brain cells?
Probably yes, in one small region, at a low rate. A 2025 Science paper found dividing neural progenitor cells in adult human hippocampus using single cell sequencing, which is the strongest direct evidence so far after a seven-year argument. Nobody has shown you can increase it deliberately or that doing so would change anything you'd notice.
Does brain training work?
It works for the thing you train, and that effect can last a decade. In ACTIVE, reasoning and speed training were still measurable ten years later. Evidence that gains transfer to untrained abilities or to everyday performance is weak, and commercial claims routinely exceed it.
Is neuroplasticity lost with age?
It appears to be reduced rather than lost. 60-year-olds in the juggling study learned the skill and showed structural brain changes, less proficiently than 20-year-olds but clearly. The more useful finding is that the changes reversed when practice stopped, in both age groups.
Which single intervention has the best evidence?
For risk reduction across a population, addressing hearing loss. It's the largest modifiable factor in the 2024 Lancet Commission accounting, and the ACHIEVE trial showed 48 percent slower decline in the higher-risk subgroup, though not in the overall sample.
How long do brain changes from training last?
Structural gray matter changes appear to fade within about three months of stopping, based on the juggling studies. Behavioural gains from cognitive training last much longer, up to ten years in ACTIVE. Those are two different things being measured, which is worth keeping separate.
Sources
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- Michiels L, Delva A, van Aalst J, et al. Synaptic density in healthy human aging is not influenced by age or sex: a 11C-UCB-J PET study. NeuroImage. 2021;232:117877. DOI: 10.1016/j.neuroimage.2021.117877
- Sorrells SF, Paredes MF, Cebrian-Silla A, et al. Human hippocampal neurogenesis drops sharply in children to undetectable levels in adults. Nature. 2018;555(7696):377-381. DOI: 10.1038/nature25975
- Boldrini M, Fulmore CA, Tartt AN, et al. Human hippocampal neurogenesis persists throughout aging. Cell Stem Cell. 2018;22(4):589-599.e5. DOI: 10.1016/j.stem.2018.03.015
- Moreno-Jiménez EP, Flor-García M, Terreros-Roncal J, et al. Adult hippocampal neurogenesis is abundant in neurologically healthy subjects and drops sharply in patients with Alzheimer's disease. Nat Med. 2019;25(4):554-560. DOI: 10.1038/s41591-019-0375-9
- Dumitru I, Paterlini M, Zamboni M, et al. Identification of proliferating neural progenitors in the adult human hippocampus. Science. 2025;389(6755):58-63. DOI: 10.1126/science.adu9575
- Draganski B, Gaser C, Busch V, Schuierer G, Bogdahn U, May A. Neuroplasticity: changes in grey matter induced by training. Nature. 2004;427(6972):311-312. DOI: 10.1038/427311a
- Boyke J, Driemeyer J, Gaser C, Büchel C, May A. Training-induced brain structure changes in the elderly. J Neurosci. 2008;28(28):7031-7035. DOI: 10.1523/JNEUROSCI.0742-08.2008
- Woollett K, Maguire EA. Acquiring "the Knowledge" of London's layout drives structural brain changes. Curr Biol. 2011;21(24):2109-2114. DOI: 10.1016/j.cub.2011.11.018
- Cabeza R. Hemispheric asymmetry reduction in older adults: the HAROLD model. Psychol Aging. 2002;17(1):85-100. DOI: 10.1037/0882-7974.17.1.85
- Reuter-Lorenz PA, Park DC. How does it STAC up? Revisiting the scaffolding theory of aging and cognition. Neuropsychol Rev. 2014;24(3):355-370. DOI: 10.1007/s11065-014-9270-9
- Erickson KI, Voss MW, Prakash RS, et al. Exercise training increases size of hippocampus and improves memory. Proc Natl Acad Sci USA. 2011;108(7):3017-3022. DOI: 10.1073/pnas.1015950108
- Firth J, Stubbs B, Vancampfort D, et al. Effect of aerobic exercise on hippocampal volume in humans: a systematic review and meta-analysis. NeuroImage. 2018;166:230-238. DOI: 10.1016/j.neuroimage.2017.11.007
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- Lin FR, Pike JR, Albert MS, et al. Hearing intervention versus health education control to reduce cognitive decline in older adults with hearing loss in the USA (ACHIEVE): a multicentre, randomised controlled trial. Lancet. 2023;402(10404):786-797. DOI: 10.1016/S0140-6736(23)01406-X
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Funding Transparency
This article received no funding. Longevity Science Daily has no commercial relationship with any manufacturer of cognitive training software, hearing devices, supplements or brain imaging services mentioned here. No sources were compensated. The author has no financial interest in any product or company named.
Worth knowing about the underlying research: the ACHIEVE trial received in-kind support in the form of hearing aids and equipment from a manufacturer, which is disclosed in the paper and is standard for device trials, and which is a reason to weight the prespecified overall null result at least as heavily as the subgroup finding. The commercial brain training sector has funded a substantial share of published training research, which is the context for the 2016 consensus review finding that marketing claims outrun the evidence. The Alzheimer's Association funded and ran US POINTER, and reported the results at its own conference before journal publication.
Every figure above was read in the primary publication or its abstract on the journal or PubMed page. Where two studies disagree, both are named rather than the convenient one. Two claims were dropped during research because the number appeared only in secondary reporting and the primary source could not be resolved.
Related Reading
- Brain Health and Mental Flexibility: Why Learning Feels Harder as We Age
- Cognitive Longevity
- The Exposome and Brain Aging
- Sleep and Aging
- Exercise and Longevity: The Zone 2 Case
- Social Connection and Longevity
Written with the help of AI tools, shaped and verified by humans who care about getting this right. Every number here was checked against the primary publication rather than a summary of it.
This article is for information only and is not medical advice. Concerns about memory or cognition belong with a clinician who can examine you.