Old Brains, New Tricks
How Neuroplasticity Can Help Your Brain Improve Any Age – And How It Can Play a Key Role in Dementia Prevention
I am amazed by our innate ability to learn. When children are young, they absorb new concepts and learn new skills every day. That’s expected, and for most of the last century, scientists believed our brains did most of their learning from birth to around age 25.
But more recent research has shown this learning doesn’t really stop, even if it’s sometimes tempered by age, genetics or physical factors. I’ve observed this phenomenon at work in the lives of my patients, who acquire new skills or knowledge at every phase of life. They take up pickleball, study a new language or learn to play a musical instrument. Through focus, dedication and time, a patient masters Rachmaninoff’s piano concerto or learns to converse in French!
It’s proof of something science didn’t really understand until recently: Neuroplasticity, our brain’s ability to modify itself in response to experience, lasts beyond our youth.
What is neuroplasticity?
Our understanding of neuroplasticity has exploded in the last 20 years. Essentially, our brain is a large network of neurons — about 90 billion of them, we think. In most basic terms, neurons are communication cells, transmitting information and actions to drive learning, memory and regulation of bodily functions. They transmit sensory input from the external world, send motor commands to our muscles and drive all the involuntary processes in our bodies that keep us living and breathing.
Consider foreign languages. There’s considerable research around first and second language learning, but scientists believed until recently that true command of a language could only be gained when the language was introduced at an early age. This thinking (called critical period hypothesis) suggests that early immersion is key.
But newer research is challenging this. Neural changes can occur even in older learners if the intensity and frequency are substantial. In fact, the science now suggests that earlier theories are probably wrong — our brains can learn a second language even late in adulthood, in a manner similar to childhood learning.
Acquiring a second language can improve our whole-brain connectivity in ways that we didn’t know until recently. People who speak two languages have stronger connections between different parts of their brain than people who speak one. The connections are better when you learn that second language as a child, but they still develop when we learn as adults.
How Learning Works
What’s going on in our brains when we learn a second language (or any new skill)? When we encounter new or important information, the connections in our brain literally get rewired. These connections are called synapses, which link neurons to neurons. With learning, some synapses strengthen while others weaken. New language acquisition, for example, creates connections between the parts of our brain that handle what we hear (auditory perception), our working memory (transient recall) and our executive functions.
These newer and more substantial connections require sustained emphasis to form. We don’t learn a new thing from just doing it once, and neuroplasticity doesn’t do shortcuts. But the potential for brain growth and change is there. What’s more, brains that are constantly challenged become more adaptable, making growth and change easier..
The Challenge of Change
Of course, neuroplasticity has its limitations, aging amongst them.
Our brain produces nearly 700 new neurons a day in our hippocampus (the center of our emotion, memory and autonomic nervous system). This process is called neurogenesis, which slows down as we age. Our synaptic density – the number of neural connections we have in the brain – may also decline, though not usually until our 70s.
We want to keep this decline from happening as long as possible, which helps to prevent dementia and other age-related brain conditions.
In essence, advanced dementia is the death of neuroplasticity. Synaptic dysfunction is an important element of Alzheimer’s Disease, which accounts for almost 70% of dementia cases in this country. When Alzheimer’s takes hold, three things happen:
- Neurons are lost
- Connections between neurons break down
- Neuroplasticity stops functioning
These changes manifest in all-too-familiar symptoms: memory problems, mood swings, loss of interest, social withdrawal, trust issues, anger, sleep troubles, wandering and delusions. In those suffering from dementia, the brain’s connections are disconnecting, and the system engineered to manage and update those connections is offline.
Dementia isn’t just cognitive decline; it’s cognitive decline combined with the loss of our ability to compensate for it. If neuroplasticity is our body’s ability to adapt, then late-stage dementia is the failure of that adaptive system.
Stimulating neuroplasticity in dementia cases
But there’s hope – and evidence – that neuroplasticity can also help in dementia cases. Neuroplasticity isn’t just for learning. It’s also an important response to injury, allowing us to adapt.
For example, in traumatic brain injuries where there is significant damage to brain tissue, neurons will attempt to form new connections to maintain important functions. This can happen after a concussion from a car wreck or sports injury. The process is called synaptogenesis. Think of this as your brain drawing a new map to old locations. Synaptogenesis occurs throughout our life, even when we’re in our 70s and 80s.
Can we enhance our brain plasticity to prevent or slow down dementia? The short answer is yes. Unfortunately, the science is complex, and our understanding of these processes is still at an early stage.
How we encourage neuroplasticity to fight dementia
But we are learning. We have good evidence that some cognitive training, specifically speed training, can reduce instances of dementia. In a 20-year-long study, researchers found that speed training – in this case, differentiating between two objects on a screen in shorter and shorter intervals – was associated with a 25 percent lower rate of dementia 20 years later.
We don’t understand why this approach worked (three other cognitive training approaches in the same study did not result in lower rates), but it’s a sign that we may be able to train our brains to resist dementia.
In people in the early or middle stages of dementia, cognitive stimulation therapy (CST) shows promise in delaying further onset. CST, usually done in a group setting, is designed to leverage neuroplasticity to improve dementia outcomes. It can include puzzles, games, playing instruments or group conversation. It has a heavy socialization component. There are a dozen studies that back this approach in dementia care.
Researchers are also looking at the positive effect exercise has on cognition and neuroplasticity. We know that exercise protects and enhances our brain – even small amounts of exercise can reduce dementia risk.
There is a mix of both animal and human studies that show the benefits of aerobic and strength training. Exercise helps our brain create new neurons and stimulates neuroplasticity. It improves blood flow in the brain, which boosts multiple neurologic processes.
Exercise also stimulates our body to produce Brain-Derived Neurotrophic Factor (BDNF), a key chemical component in neuroplasticity and in neuronal health in general. It helps produce PGC-1alpha, which plays a critical role in mitigating neurodegenerative disorders like dementia and Parkinson’s. And it has an anti-inflammatory effect, which slows down the progression of such conditions.
Scientists are researching other treatments aimed at helping stimulate our neuroplasticity. Studies in brain stimulation techniques through Transcranial Magnetic Stimulation, Deep Brain Stimulation and Transcranial Electric Stimulation have shown some early promise as have other experiments with augmented and virtual reality.
Pharmaceutical approaches
Not surprisingly, most of our pharmaceutical approaches to dementia treatment center around restoring or preserving our neuroplastic abilities. The two most common drug therapies – anti-amyloid monoclonal antibodies and cholinesterase inhibitors – tackle the challenge differently, but both aim to encourage neuroplasticity.
Anti-Amyloid drugs are designed to reduce amyloid plaques by leveraging the immune system. Alzheimer’s Disease results from the accumulation of amyloid and other proteins in neural tissue. These proteins cause nerve tangles, thereby disrupting communications and hindering synapse formation. Inevitably, these alterations impair neuroplasticity. Anti-amyloid drugs work to decrease amyloid protein in the brain and therefore to prevent the formation of new tangles.
Cholinesterase inhibitors work by boosting the levels of acetylcholine, an important neurotransmitter that carries signals from neuron to neuron. The deterioration of neurons in the brain from Alzheimer’s Disease results in weakening of that signal. Cholinesterase inhibitors can help to amplify the signal once more, keeping brain connections strong.
Taking advantage of neuroplasticity
Neuroplasticity may ultimately be powerful medicine for people with dementia, but it’s a tool for anyone who wants to live better and longer. How can we make sure this tool is working on our behalf? Start with these five tips.
Get exercise. Physical activity, as mentioned, is one of the most powerful neuroplastic tools available. Studies show that regular physical activity can lower dementia risk by up to 45% and improve overall cognition. In particular, aerobic exercise promotes neurogenesis and preserves our brain structure. Even modest activity – like walking several thousand steps a day – has been linked to delayed memory decline.
Good sleep is brain maintenance. During sleep your brain repairs itself, consolidates memories and clears waste products. Poor sleep is strongly associated with faster cognitive decline and increased dementia risk. Research also shows that inconsistent or low-quality sleep correlates with worsening cognitive performance over time. Good sleep is essential to maintain neuroplasticity.
Manage stress to brain function. Chronic stress disrupts brain networks involved in memory and decision-making. It also contributes to neurodegenerative changes when combined with poor sleep and inactivity. Regular stress-management practices like mindfulness, exercise and social connection help preserve resilience and rewiring.
Eat for brain health. Research on Mediterranean-style diets, shows they can significantly slow aging and atrophy of the brain by up to 50% in some populations. These diets emphasize vegetables, healthy fats, lean proteins and polyphenol-rich foods (think berries) that reduce inflammation and support neural health.
Nurture positive social connections. Just like learning a language, social interactions challenge us and help cultivate neuroplasticity. Studies show increases in activity in key areas of our brains when we interact positively with others and may explain why we can struggle cognitively after the death of a partner. Negative social interactions can have a negative effect; if a relationship causes you stress, it may not be helping your brain.
Challenge your brain regularly. Finally, neuroplasticity thrives on novelty and challenge. Cognitive training – especially activities that demand speed, attention and problem-solving – has been shown to reduce dementia risk by about 25% over time. Broader lifestyle trials confirm that combining mental stimulation with exercise and diet leads to measurable improvements in cognitive performance.
Our brain is complex, but it’s good to know it doesn’t stop growing when we do. It adapts over our lifetimes, always seeking to maximize our cognitive and neurologic function. With proper care and a healthy lifestyle, we can leverage this natural process to help us as we age. So take care of your brain and keep stimulating it.