Neuroplasticity Across the Lifespan: How the Brain Rewires Itself and What Drives It
The adult brain was long thought to be fixed after early development. It is not: connections between neurons keep strengthening and weakening with experience throughout life,2 and some brain regions change in size with how they are used.1 This article covers what is established, what is still disputed, and what has been shown to change the adult brain.
- The adult brain keeps changing: the long-term strengthening and weakening of synapses (LTP and LTD) occurs at possibly every excitatory synapse in the mammalian brain.2
- Whether adults keep making new neurons in the hippocampus is disputed: a 1998 study found new neurons in adults,4 a 2018 study found the process drops to undetectable levels by adulthood,5 and another 2018 study found it preserved in healthy older people.6
- Use reshapes structure: London taxi drivers had larger posterior hippocampi than controls, and volume tracked years on the job.1 In older adults, a year of aerobic exercise training enlarged the hippocampus and improved memory.7
- Cognitive reserve, the brain's resilience against damage, may be built by education, work and leisure activities across life, according to epidemiological studies.8
- Sleep renormalizes synaptic strength, which may explain its benefits for memory.3
In 1998, researchers reported new neurons forming from dividing progenitor cells in the adult human hippocampus.4 In 2000, a study of London taxi drivers found larger posterior hippocampi than in controls, with volume tracking time spent driving a taxi.1 Since then, the question of how much new-neuron formation continues in adults has become one of the field's main disputes.5,6
The Neurogenesis Debate in Detail
The 1998 evidence came from brain tissue donated by patients who had been given bromodeoxyuridine, a compound that labels DNA in dividing cells; labelled cells carrying neuronal markers showed that new neurons were being generated from dividing progenitor cells in the hippocampus.4 The 2018 study that challenged it found that dividing progenitors and young neurons in the dentate gyrus decline sharply during the first year of life, with only a few isolated young neurons left by ages 7 and 13.5 Another 2018 study, which examined whole hippocampi from healthy people aged 14 to 79, reached the opposite conclusion: healthy older people without cognitive impairment or psychiatric disease showed preserved neurogenesis, although older brains had less blood-vessel growth and plasticity in part of the region.6
The taxi-driver study showed that structural change can involve trade-offs. A more anterior part of the hippocampus was larger in controls than in drivers, and with more years on the job, posterior volume rose while anterior volume fell. The authors concluded that the healthy adult brain is capable of local structural change in response to environmental demands.1
Forms of Neuroplasticity
Most adult plasticity happens at synapses. Long-term potentiation (LTP) and long-term depression (LTD), the lasting strengthening and weakening of synaptic transmission, are found at possibly every excitatory synapse in the mammalian brain, and they come in several forms with different mechanisms.2 These mechanisms are not one process: they vary with the synapses and circuits involved, and they contribute to experience-dependent changes in brain function.2
Sleep as the Plasticity Consolidation Window
The synaptic homeostasis hypothesis holds that waking experience strengthens synapses overall and that, during sleep, spontaneous activity renormalizes synaptic strength; this down-selection may explain sleep's benefits for memory acquisition, consolidation and integration.3
The hypothesis frames sleep as the price the brain pays for plasticity: learning about the day's environment strengthens connections throughout the brain, which raises cells' needs for energy and supplies, lowers the signal-to-noise ratio and saturates the capacity to learn, until sleep resets the balance.3
What Trials Show You Can Change
Exercise. In a randomized controlled trial of 120 older adults, a year of aerobic exercise training enlarged the anterior hippocampus by 2%, effectively reversing one to two years of age-related shrinkage, and improved spatial memory.7 Larger gains in hippocampal volume went with higher blood levels of BDNF, a growth factor involved in forming new neurons.7
Cognitive training. Training improves mainly what you practise. In the ACTIVE trial, 2,832 independent adults aged 65 to 94 received ten sessions of memory, reasoning or speed-of-processing training, and a random 60% were offered four booster sessions 11 months later.9 Each type of training improved the ability it targeted, with gains lasting at least two years; right after training, 87% of the speed group, 74% of the reasoning group and 26% of the memory group showed reliable improvement.9 Ten years later, at an average age of 82, about 60% of trained participants were at or above their starting level of self-reported everyday function, against 50% of controls.10
Combining habits. In the FINGER trial of older adults at raised risk of dementia, two years of diet guidance, exercise, cognitive training and vascular risk monitoring produced a small but statistically significant cognitive benefit over general health advice: test-battery scores rose by 0.20 standard units against 0.16.11 The authors concluded that such a programme could improve or maintain cognitive function in at-risk older people.11
Putting It Into Practice
The evidence points to a mix rather than a single trick. Regular aerobic exercise has changed brain structure in a randomized trial; structured training improves the specific skills it targets; and a combined programme of diet, exercise, training and risk-factor care gave older adults at risk a modest cognitive benefit. Education, demanding work and leisure activities in later life are linked to greater cognitive reserve in epidemiological studies, which suggests that staying mentally engaged matters across the whole lifespan.8
References
- 1Maguire EA, et al. "Navigation-related structural change in the hippocampi of taxi drivers." Proc Natl Acad Sci U S A. 2000;97(8):4398-403. PubMed · DOI
- 2Malenka RC, Bear MF. "LTP and LTD: an embarrassment of riches." Neuron. 2004;44(1):5-21. PubMed · DOI
- 3Tononi G, Cirelli C. "Sleep and the price of plasticity: from synaptic and cellular homeostasis to memory consolidation and integration." Neuron. 2014;81(1):12-34. PubMed · DOI
- 4Eriksson PS, et al. "Neurogenesis in the adult human hippocampus." Nat Med. 1998;4(11):1313-7. PubMed · DOI
- 5Sorrells SF, et al. "Human hippocampal neurogenesis drops sharply in children to undetectable levels in adults." Nature. 2018;555(7696):377-381. PubMed · DOI
- 6Boldrini M, et al. "Human Hippocampal Neurogenesis Persists throughout Aging." Cell Stem Cell. 2018;22(4):589-599.e5. PubMed · DOI
- 7Erickson KI, et al. "Exercise training increases size of hippocampus and improves memory." Proc Natl Acad Sci U S A. 2011;108(7):3017-22. PubMed · DOI
- 8Stern Y. "Cognitive reserve in ageing and Alzheimer's disease." Lancet Neurol. 2012;11(11):1006-12. PubMed · DOI
- 9Ball K, et al. "Effects of cognitive training interventions with older adults: a randomized controlled trial." JAMA. 2002;288(18):2271-81. PubMed · DOI
- 10Rebok GW, et al. "Ten-year effects of the advanced cognitive training for independent and vital elderly cognitive training trial on cognition and everyday functioning in older adults." J Am Geriatr Soc. 2014;62(1):16-24. PubMed · DOI
- 11Ngandu T, et al. "A 2 year multidomain intervention of diet, exercise, cognitive training, and vascular risk monitoring versus control to prevent cognitive decline in at-risk elderly people (FINGER): a randomised controlled trial." Lancet. 2015;385(9984):2255-63. PubMed · DOI
