Neuroscience 101

March 04, 2017

Neuroscience 101

How The Brain Works

Learning, Storing and Recalling Information

By Dr. Shawn Watson, Co-founder and CEO, Senescence Life Sciences

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 the neurotransmitters will 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.

Within the brain, 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. Importantly, it is within the synapses of our brain (all ~100,000,000,000,000 of them!) where all of our memories are stored.

What Happens As We Age

What Happens As We Age
As the brain ages, our ability to learn, store and recall information gradually declines. At a cellular level, this means that as we age we 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, it would mean 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 twenties, becomes apparent in our early forties and accelerates in our mid-sixties and beyond.
It is important to note that the natural decline in cognitive function as we age is not the result of our brain cells dying. This is a common misconception that seems to persist within popular media. Generally speaking, neuronal death within the brain is only associated with pathological diseases like Alzheimer’s and Parkinson’s.

Why The Brain Ages

Why The Brain Ages - The Free Radical Theory Of Aging

The Free Radical Theory of Aging (FRTA) is a theory widely accepted amongst the scientific community that explains why organisms and tissues, including the brain, age. The theory is based upon the fact that cellular metabolism (the process that gives our cells the energy to function) produces harmful by-products that damage the cell. These by-products take the form of free radicals, which are defined as any atoms or molecules that have a single unpaired electron within their outer shell, making them highly reactive. Our cells (particularly our neurons) have, however, developed a plethora of defenses against these free radicals, both to disengage them immediately and to repair the damage that they cause. Despite these considerable defences, as we age there is a shift in the balance between rates of damage and rates of repair, resulting in the build-up of harmful compounds (just like the sludge that builds within a car engine over time).

Our neurons are extremely unique cells, unlike anything else in our body in regards to their energetic demands. They operate in a finely-tuned metabolic environment and use an incredible amount of energy - with oxygen as their fuel. In terms of metabolism, our brain makes up only 2% of our body mass but consumes 20% of our oxygen. This equates to your brain generating between 10 and 25 watts of power - enough energy to power a light bulb. With such significant energetic demands, our neurons experience arguably the highest rates of free radical production in our body.

While other molecular components of neurons can be attacked by free radicals, lipids (fats) are particularly susceptible due to their sheer abundance in the brain (60% of the brain is fat!). Scientists call this process "lipid peroxidation" and recent lines of evidence, including studies by Senescence Life Sciences, have shown that this process is key to understanding why a neuron’s ability to conduct electrical signals changes with age. Luckily, neurons are extremely resilient and have natural repair mechanisms capable of combating the ongoing damage. These capabilities, however, begin to change with age, and we start to see a gradual buildup of lipid damage within the cell and a resulting reduction in the transmission abilities of our neurons. Ultimately, as previously mentioned, these changes are thought to be responsible for the natural decline in cognitive capabilities of the human brain.

The previous sections stress the importance of supporting and regulating neuronal repair mechanisms within the aging brain. It is important to remember that neurons do not replicate, divide or renew themselves. For all intents and purposes, with a few exceptions aside, the number of neurons you are born with is the number you die with… so take care of them!


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