Brain Plasticity and Environmental Manipulations That Can Counteract Brain Pathology and Aging

Written by Brett Weiss

August 2019

Image by Gordon Johnson from Pixabay

Brain plasticity, the ability of neurons of the cerebrum to change structure and function with experience, constitutes a remarkable feature of cerebral neurons.  How does this ability evolve over the lifespan of neurotypical individuals?  Also, how might environmental manipulations facilitate enhanced brain plasticity in pathology and older age?  The aims of this article entail illustrating how brain plasticity changes over time and offering possible solutions for improving brain plasticity with pathology and age.

Not so long ago, most mainstream neuroscientists contended that neuroplasticity was limited to an early period in childhood– a “critical period.”  The science of brain plasticity has shown since that brain remodeling can take place on large scales at any age (Merzenich et al., 2014).  The main differences in brain plasticity from younger to older age relate to the mechanisms that the brain uses to regulate plasticity.  For instance, in the young brain, inputs engage competitive plasticity processes.  In older brains, behavioral context and outcomes function to regulate plasticity.

In early childhood during the “critical period,” plasticity-enabling mechanisms in the brain are always “on.”  In older children and adults, changes in control of the release of “neuro-modulatory neurotransmitters” take place in comparison to the “critical period.”  The properties of the receptors that respond to these neurotransmitters change as well to enable a moment-by-moment control of change in older children and adults.  In this way, only specific contextual conditions trigger plasticity such that enduring changes in connection strength occur with the behavioral outcome.  Hence, in older children and adults, specific contextual conditions correlate with a behavioral outcome; and thus, brain connections get strengthened.  The “neuro-modulatory neurotransmitter” acetylcholine gets released from the basal nucleus of Meynert under conditions of focused attention (Merzenich et al., 2014).  In the cortex, acetylcholine positively enables plasticity with 1) amplifying only anticipated inputs and 2) weakening non-anticipated inputs, which include those inputs that may have previously effectively excited neurons before the learning-induced changes.  Another “neuro-modulatory neurotransmitter” involved in brain plasticity outside of the “critical period,” noradrenaline, gets released from the locus coeruleus and amygdala.  In the cortex, noradrenaline amplifies neuronal activity, increasing the level of excitability.  In that respect, a “surprising” input will drive enduring representational changes (Merzenich et al., 2014).  The last “neuro-modulatory neurotransmitter” mentioned, dopamine, gets released from the ventral tegmental area and substantia nigra to enable brain plasticity.  These structures release dopamine when the brain predicts occurrence of an input and then receives that input (reward) or when the brain predicts behavioral success and then achieves that success (rewards itself) in a learning cycle.  Inputs that predict the reward or which are highly correlated with occurrence of the reward get selectively strengthened in the brain (Merzenich et al., 2014).

The psychiatric disorder of schizophrenia will be used in order to illustrate a brain pathology for which neuroscientists have developed methods in order to enhance brain plasticity.  Research on the disorder currently shows marked neurocognitive and social cognitive impairments in schizophrenia (Merzenich et al., 2014).  Deficits related to perception, processing speed, working memory, executive function, attention, social cue perception, and action control associate with poor societal and occupational outcome (Merzenich et al., 2014).  Because these deficits do not encompass psychotic symptoms, antipsychotic medications do not significantly ameliorate these impairments.  For example, second-generation dopamine-agonist antipsychotics show no advantage over first-generation medicines in treating cognitive deficits from schizophrenia (Merzenich et al., 2014).  Merzenich et al. (2014) hypothesize that these impairments in perception and cognition facilitate a breakdown in working memory with poor social outcomes.  The same group believes that training which improves these neurological abilities may contribute to working memory and “neuro-modulatory neurotransmitter” system function.  In essence, training these neuro-modulatory systems could have significant therapeutic value through improvement of brain plasticity.

In order to target perceptual, cognitive, social, and motor control impairments in the disorder, neuroscientists have generated computerized cognitive training programs.  The training programs give specific attention to training of social cognition as poor social cognition has been linked to poor functional outcomes in schizophrenia.  Poor functional outcomes associated with impairments in social cognition include occupational status, community functioning, independent living, and quality of life (Merzenich et al., 2014).  The social cognitive training, called “SocialVille,” utilizes socially-relevant stimuli in tasks targeting affective or facial expression perception, social cue perception, and theory of mind (predicting the thoughts, beliefs, and goals of others).  Different combinations of this type of training have been deployed to patients with schizophrenia with improvements in the targeted cognitive domains.  Although more research is needed, it appears that these computer-based cognitive training programs hold promise in improving brain plasticity and social function in patients with schizophrenia (Merzenich et al., 2014).

Adult neurogenesis, the generation of new neurons in the adult brain, plays a crucial role in neural plasticity in the aging population.  New neurons in the adult brain originate in the dentate gyrus of the hippocampus, an area important for acquisition of new memories.  Voluntary running along with exposure to sensory, cognitive, motor, and socially enriched conditions (enriched environment) stimulate adult hippocampal neurogenesis (Sale et al., 2014).  The new neurons which come from adult neurogenesis integrate in local circuits and receive and establish synaptic contacts.  These new neurons are also particularly susceptible to synaptic plasticity which strengthens synapses (LTP). 

Many studies have found that an enriched environment with lots of cognitive stimulation promotes survival of new neurons from adult neurogenesis.  Voluntary aerobic exercising promotes a higher-level generation of new neurons through adult neurogenesis in comparison to a sedentary lifestyle.  Hence, a combination of enriched environment with an aerobic exercise regimen may facilitate enhanced brain plasticity through adult neurogenesis (Sale et al., 2014).

Brain plasticity, which implies pliability and malleability of the brain, can be rescued to different degrees in pathology and aging.  The preservation of brain plasticity implies maintenance of learning and memory abilities along with various aspects of cognition.  As research progresses, enriched environments of intellectual stimulation along with aerobic exercise regimens may become optimized to facilitate preservation of cognition and may even allow cognitive enhancement.  Medications have necessity in treating psychological dysfunction; however, they do not necessarily treat the core symptoms that lead to poor social and societal outcomes in pathology.  Rigorous computerized training may soon supplement medications in order to treat the full gamut of symptoms associated with pathology from psychiatric disorders and aging.


Merzenich MM, Van Vleet TM, & Nahum M (2014).  “Brain plasticity-based therapeutics.”  Front Hum Neurosci.  8(385).

Sale A, Berardi N, & Maffei L (2014).  “Environment and Brain Plasticity: Towards an Endogenous Pharmacotherapy.”  Physiol Rev.  94: 189-234.

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