Neuroplasticity: How the Brain Changes and What Supports It

By Peter Benson, Cognitive Enhancement Researcher  ·  Updated October 2026  ·  Citations re-verified

Short answer: Neuroplasticity is the brain’s ability to change its connections with experience, and it continues throughout adult life. The best-supported ways to support it are regular aerobic exercise, learning things that genuinely challenge you, enough sleep and keeping chronic stress down. Supplement evidence is much weaker and mostly comes from animals.

For much of the 20th century, the adult brain was thought to be largely fixed. That view has gone: the adult brain keeps changing its connections in response to what you do, learn and experience. “Neuroplasticity” has since become a marketing word attached to games, supplements and courses, most of which have little evidence behind them.

This guide explains how the brain changes, which everyday levers have human evidence, and where the claims, including about supplements, outrun the research. It ends with my own routine, which I have not measured. It is part of the Brain Health & Longevity hub.

How neuroplasticity works

Strengthening connections. When two connected neurons are repeatedly active together, the connection between them strengthens, a process called long-term potentiation. It is the best-studied cellular basis of learning and memory. Connections that are rarely used weaken, and some are removed altogether, which makes the remaining circuits more efficient.

BDNF. Brain-derived neurotrophic factor is a protein that supports the growth and survival of neurons and helps connections strengthen. It is released in response to activity, and exercise raises it: a meta-analysis of 29 studies found that a single exercise session raised blood BDNF moderately, and regular exercise raised resting levels slightly (Szuhany et al., 2015). One caution runs through this research: human studies measure BDNF in blood, and how well that reflects the brain is uncertain.

New neurons. In mice, running roughly doubled the number of new cells in the hippocampus, a memory area, and improved learning (van Praag et al., 1999). New neurons were first shown in the adult human hippocampus in 1998 (Eriksson et al., 1998). How much this continues into later life has been argued over: some studies of post-mortem brain tissue find very few new neurons in adults, others find them into old age. A 2026 Nature study of 38 donated brains, analysing nearly 356,000 cells, found stem cells, precursor cells and immature neurons in adult hippocampi, fewer immature neurons in Alzheimer’s disease, and a distinct profile in “SuperAgers” over 80 with exceptional memory (Disouky et al., 2026). That strengthens the case that the process persists in adults, but the groups were small, the tissue is post-mortem, and it can’t show how many new neurons mature or what they contribute to memory. Most of the practical advice on this page doesn’t depend on settling that question.

What supports neuroplasticity in adults

1. Aerobic exercise. In a trial of 120 older adults, a year of walking three times a week increased the size of the hippocampus by about 2%, while a stretching group lost about 1.4%; memory improved in both groups (Erickson et al., 2011). A meta-analysis of 14 trials with 737 people found no significant effect on total hippocampal volume, but a benefit on the left side that came mainly from preventing shrinkage rather than growth (Firth et al., 2018). So exercise looks protective, though more modest than the “2% bigger” headline suggests, and structural changes don’t necessarily bring equal improvements in memory. Guidelines recommend about 150 minutes of moderate activity a week; no specific dose has been shown best for the brain. See exercise and BDNF.

2. Learning that challenges you. Plasticity is use-dependent: the circuits you use are the ones that change. Active learning, such as retrieving what you’ve learned rather than re-reading it, or practising a skill just beyond your current level, usually improves retention more than passive review. That fits experience-dependent plasticity, though these studies measure learning, not synapses. Commercial brain-training games are the cautionary case: a major review found they improve performance on the trained tasks, with little evidence of transfer to everyday thinking (Simons et al., 2016). See the neuroscience of learning.

3. Sleep. Sleep helps consolidate memories formed during the day. One influential theory holds that sleep also scales back the connections strengthened while awake, keeping the brain ready to learn again; it is well supported in animals but still a hypothesis (Tononi & Cirelli, 2014). Whatever the mechanism, people who are short of sleep learn and remember worse. See sleep architecture.

4. Keeping chronic stress down. In animals, prolonged stress hormones shrink neuron branches in the hippocampus and prefrontal cortex, and in humans chronic stress and depression are linked with smaller hippocampal volume (McEwen et al., 2016). Much of the animal damage reverses when stress ends. Short-term stress is a normal response and doesn’t necessarily cause lasting change, though it can temporarily affect attention and memory depending on how intense it is. See chronic stress and cortisol.

Neuroplasticity interventions ranked by evidence

🟢 Stronger or replicated evidence  ·  🟡 Limited, mixed or preliminary evidence  ·  🔴 Not established or not supported

Supplements and neuroplasticity: what the evidence shows

Supplement marketing often borrows the language of brain structure: “grows new neurons”, “builds synapses”. For every compound below, those structural effects come from cell or animal studies. What exists in humans is a handful of trials measuring memory or test scores.

Bacopa. The best human evidence of the four. In one 12-week trial, Bacopa improved memory measures compared with placebo (Roodenrys et al., 2002), and several similar trials agree that the effect is small. See the Bacopa guide.

Lion’s Mane. It stimulates nerve growth factor in cell and animal studies. The key human trial gave it to 30 Japanese adults with mild cognitive impairment for 16 weeks; their scores improved compared with placebo and fell again after they stopped (Mori et al., 2009). Trials in healthy adults are small and mixed. See Lion’s Mane benefits.

Omega-3 DHA. DHA is a building block of nerve cell membranes. One trial found 900mg a day for six months improved learning and memory in older adults with memory complaints (Yurko-Mauro et al., 2010), but most trials in healthy people have found no benefit. See the omega-3 DHA guide.

Magnesium L-threonate. It raised brain magnesium and the number of synapses in rats (Slutsky et al., 2010). In humans there are now two small trials. One, in 44 adults aged 50 to 70 over 12 weeks, found better composite cognitive scores; it was funded by the product’s maker (Liu et al., 2016). The other gave 2g a day of Magtein or placebo for six weeks to 100 adults aged 18 to 45 who were unhappy with their sleep; the overall cognition score and reaction time improved more than with placebo, but wearable sleep measures showed no difference (Lopresti & Smith, 2026). The trial’s “7.5 years younger cognitive age” is a calculated test-score estimate, not a reversal of brain ageing. Neither trial measured synapses, and independent replication is still needed. See magnesium L-threonate.

Trial lengths of 12 to 16 weeks are a reference for how long these studies ran, not a guaranteed timeline. Supplements can interact with medicines; check with a doctor or pharmacist if you take any.

Frequently asked questions

Scientific references