By Dr. Shawn Watson, CEO & Co-Founder of Senescence Life Sciences, Creators of EDGE Brain Supplement
At the most basic level, the human brain is a network of cells (neurons) working together to process, learn, retain and recall information. When we experience an external stimulus such as a sight, sound or taste, an electrical signal travels to our brain, passing from neuron to neuron.
There are, however, small gaps between each neuron called synapses, where the electrical signal is converted into a chemical signal. These chemical signals are called 'neurotransmitters', and neurotransmitters travel across the synapse that separates one neuron from another. Once these neurotransmitters cross the synapse and reach the connecting neuron, the electrical signal will be restarted and the process repeats itself.
These synapses are incredibly dynamic and actively change depending on how frequently they’re used. Many variables can cause a synapse to become stronger or weaker. For example, as we learn a specific task - say flipping a fried egg with a spatula – the connections between our hand and eyes become stronger as we repeat the motion. In contrast, a professional soccer goalie needs to intentionally weaken the connections within their brain that would normally cause them to flinch away from an incoming soccer ball.
Generally speaking, the ability to strengthen or weaken a connection is called ‘synaptic plasticity,’ and defines the ‘plastic’ (malleable) nature of our brain. It is also within all ~100,000,000,000,000 of our synapses in our brain where our memories are stored.
What Happens As We Age?
As our brains age, our ability to learn, store and recall information gradually declines. At a cellular level, this means that we slowly lose the ability to create lasting changes to our synapses.
One prominent theory explaining this change focuses on an age-dependent reduction in the ability of our neurons to conduct electrical impulses. This is often referred to as a reduction in a neuron’s electrical ‘excitability’, and means that an aged neuron may be unable to respond appropriately to a given stimuli. Practically, this means that the neuron is no longer able to generate a strong enough electrical signal when required to do so.
Lacking this signal leads to an inability to substantively change the strength of a synaptic connection, thereby impairing our capacity to learn, store and recall information as we age. In humans this decline begins in our early 20's, becomes more apparent in our early 40's and accelerates in our mid-60's and beyond.