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Changing our neurological fate

How exercise and mental stimulation sharpen our senses and enhance cognitive abilities

     
                    changing-our-neurological-fate 
 
Aging diminishes our ability to process new information. After a certain point in our development, the critical period of learning closes off and our senses become less receptive to stimuli. This is exemplifed by the remarkable capacity of young children who almost effortlessly pick up a new language in their infancy, but find it much harder to grasp the basic concepts of a foreign language in University.

Synaptic plasticity is the ability of neuronal connections, called synapses, to either strengthen with increased neural activity, or to diminish when left unused. The loss of too many individual synaptic connections can lead to deterioration of important neural pathways—one of the underlying causes of many neurodegenerative diseases.

However, there may be some hope to influence our ‘fate’ of cognitive decline and to counter the loss of synaptic plasticity in the brain. Research has shown that the rate of new neuron formation is enhanced by physical activity, and that the survival of these new neurons increases when we are immersed in a constantly challenging environment.

How does this work?

Exercise has been shown to increase the rate of long-term potentiation (LTP) in the synapse, which reinforces connections between neurons within a particular pathway. Neurons require this constant stimulation and activity to stay healthy and to prevent degeneration of the neuronal circuitry. Providing an enriched environment (from, for example, activities that exercise and stimulate our bodies and minds) allows newly formed neurons to retain activity and ensures that the new pathways are maintained.

A prime mechanism behind neurogenesis—the development of new neurons—involves a protein called brain-derived neurotrophic factor (BDNF). Increased synaptic activity causes higher levels and increased expression of BDNF which, in turn, releases neurotransmitters into the synapse. When enough excitatory ionic ‘charge’ accumulates to exceed the threshold, the synapse is depolarized and the neuron fires.

As a result, any immature newborn granule cells—small underdeveloped precursor neurons—in the pathway are recruited and incorporated into the circuitry. Since the survival of mature neurons is activity-dependent, the firing threshold is lowered, making it easier for the neuron to become depolarized and excited. This enhances LTP, which ensures that the neuron will continue to fire and thus strengthen its connections with neighbouring neurons to reinforce its place in the neural pathway. This process works in much the same way as the development of ‘muscle memory’ when we learn to ride a bike, for example. We start by learning the basic movements with training wheels and, with practice, we learn to balance ourselves. Without practice and consistant reinforcement of the motor pathway, learning would not come as easily.

LTP takes place primarily in regions of the brain that are constantly being enriched with new stimuli. These areas include the dentate gyrus in the hippocampus, which is responsible for memory formation, as well as the olfactory bulb where new neurons are constantly needed to integrate new smells and senses into the brain. Recent studies have also reported the presence of neural progenitor cells in the retina—a finding that could have implications for people with impaired vision caused by diabetic retinopathy.
 
 

New research at Mount Sinai Hospital

At the Samuel Lunenfeld Research Institute of Mount Sinai Hospital , Principal Investigator Dr. Kenichi Okamoto and his team are currently developing a new method to better understand the biochemical mechanisms behind LTP and synaptic plasticity. His work involves the creation of a two-photon laser capable of visualizing several larger portions of the brain concurrently. “The laser is a cleaner method to manipulate proteins compared with current strategies, as it allows for greater precision in the study of cell function,” says Dr. Okamoto. He hopes that with further developments, he will eventually be able to see the entire brain as a whole, in action.

 
Dr. John Roder, Lunenfeld Senior Investigator and holder of a Canada Research Chair in Learning and Memory, is studying the roles of certain genes in the regulation of synaptic protein receptors and their effect on synaptic plasticity.
 
The work of Drs. Okamoto and Roder will give insight into the mechanisms behind diseases such as Alzheimer’s, Parkinson’s, and other neurodegenerative illnesses. Dr. Roder notes that the work being done is only scratching the surface, and says that “there is a lot we still do not know about the brain. Large research gaps still exist and new questions should be focused on especially prevalent and complex disorders such as autism—a polygenic disorder the causes of which are poorly understood.”
 

Although both genetic and environmental factors are at play in such matters, Drs. Okamoto and Roder both agree that we must persist to ‘challenge’ our neurons constantly despite certain genetic and age-related forces that may be beyond our control. More simply put: we must learn to use it or lose it, for our own sake.

 

 

 
 

 



 

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