Research indicates that living in areas of high pollution has serious long term health effects. Living in these areas during childhood and adolescence can lead to diminished mental capacity and an increased risk of brain damage. People of all ages who live in high pollution areas for extended periods place themselves at increased risk of various neurological disorders. Both air pollution and heavy metal pollution have been implicated as having negative effects on central nervous system (CNS) functionality. The ability of pollutants to affect the neurophysiology of individuals after the structure of the CNS has become mostly stabilized is an example of negative neuroplasticity.
Air pollution
Air pollution is known to affect small and large blood vessels throughout the body.
High levels of air pollution are associated with increased risk of strokes and heart attacks. By permanently affecting vascular structures in the brain, air pollution can have serious effects on neural functioning and neural matter. In dogs, air pollution has been shown to cause damage to the CNS by altering the blood–brain barrier, causing neurons in the cerebral cortex to degenerate, destroying glial cells found in white matter, and causing neurofibrillary tangles. These changes can permanently alter brain structure and chemistry,
resulting in various impairments and disorders. Sometimes, the effects
of neural remodeling do not manifest themselves for a prolonged period
of time.
Effects in adolescents and canines
A study from 2008 compared children and dogs raised in Mexico City (a location known for high pollution levels) with children and dogs raised in Polotitlán, Mexico (a city whose pollution levels meet the current US National Ambient Air Quality Standards). According to this study, children raised in areas of higher pollution scored lower in intelligence (i.e. on IQ tests), and showed signs of lesions in MRI
scanning of the brain. In contrast, children from the low pollution
area scored as expected on IQ tests, and did not show any significant
sign of the risk of brain lesions. This correlation was found to be
statistically significant, and shows that pollution levels may be
related to, and contribute to, brain lesion formation and IQ scores,
which, in turn, manifests as impaired intellectual capacity and/or
performance. Living in high pollution areas thus places adolescents at
risk of premature brain degeneration
and improper neural development—these findings could have significant
implications for future generations. With regard to traffic related air
pollution, children of mothers exposed to higher levels during the first
trimester of pregnancy were at increased risk of allergic sensitization
at age 1 year.
Effects in adults
There
are indications that the effects of physical activity and air pollution
on neuroplasticity counteract. Physical activity is known for its
health-enhancing benefits, particularly on the cardiovascular system, and has also demonstrated benefits for brain plasticity processes, cognition and mental health. The neurotrophine, brain-derived neurotrophic factor
(BDNF) is thought to play a key role in exercise-induced cognitive
improvements. Brief bouts of physical activity have been shown to
increase serum levels of BDNF, but this increase may be offset by increased exposure to traffic-related air pollution.
Over longer periods of physical exercise, the cognitive improvements which were demonstrated in rural joggers were found to be absent in urban joggers who were partaking in the same 12-week start-2-run training programme.
Epilepsy
Researchers in Chile found statistically-significant correlations between multiple air pollutants and the risk of epilepsy using a 95% confidence interval. The air pollutants that the researchers attempted to correlate with increased incidence of epilepsy included carbon monoxide, ozone, sulfur dioxide, nitrogen dioxide, large particulate
matter, and fine particulate matter. The researchers tested these
pollutants across seven cities and, in all but one case, a correlation
was found between pollutant levels and the occurrence of epilepsy. All
of the correlations found were shown to be statistically significant.
The researchers hypothesized that air pollutants increase epilepsy risk
by increasing inflammatory mediators, and by providing a source of oxidative stress. They believe that these changes eventually alter the functioning of the blood–brain barrier, causing brain inflammation.
Brain inflammation is known to be a risk factor for epilepsy; thus, the
sequence of events provides a plausible mechanism by which pollution
may increase epilepsy risk in individuals who are genetically vulnerable to the disease.
Dioxin poisoning
Organohalogen compounds, such as dioxins, are commonly found in pesticides or created as by-products of pesticide manufacture or degradation. These compounds can have a significant impact on the neurobiology of exposed organisms. Some observed effects of exposure to dioxins are altered astroglial intracellular calcium ion (Ca2+), decreased glutathione levels, modified neurotransmitter function in the CNS, and loss of pH maintenance. A study of 350 chemical plant employees exposed to a dioxin precursor for herbicide synthesis between 1965 and 1968 showed that 80 of the employees displayed signs of dioxin poisoning.
Of these 350 employees, 15 were contacted again in 2004 to submit to
neurological tests to assess whether the dioxin poisoning had any
long-term effects on neurological capabilities. The amount of time that
had passed made it difficult to assemble a larger cohort,
but the results of the tests indicated that eight of the 15 subjects
exhibited some central nervous system impairment, nine showed signs of polyneuropathy, and electroencephalography
(EEG) showed various degrees of structural abnormalities. This study
suggested that the effects of dioxins were not limited to initial toxicity. Dioxins, through neuroplastic effects, can cause long-term damage that may not manifest itself for years or even decades.
Metal exposure
Heavy metal exposure can result in an increased risk of various neurological diseases. Research indicates that the two most neurotoxic heavy metals are mercury and lead. The impact that these two metals will have is highly dependent upon the individual due to genetic variations. Mercury and lead are particularly neurotoxic for many reasons: they easily cross cell membranes, have oxidative effects on cells, react with sulfur in the body (leading to disturbances in the many functions that rely upon sulfhydryl groups), and reduce glutathione levels inside cells. Methylmercury, in particular, has an extremely high affinity for sulfhydryl groups. Organomercury is a particularly damaging form of mercury because of its high absorbability Lead also mimics calcium, a very important mineral in the CNS, and this mimicry leads to many adverse effects. Mercury's neuroplastic mechanisms work by affecting protein production. Elevated mercury levels increase glutathione levels by affecting gene expression, and this in turn affects two proteins (MT1 and MT2) that are contained in astrocytes and neurons. Lead's ability to imitate calcium allows it to cross the blood–brain barrier. Lead also upregulates glutathione.
Heavy metal exposure, when combined with certain genetic predispositions, can place individuals at increased risk for developing autism. Many examples of CNS pathophysiology, such as oxidative stress, neuroinflammation, and mitochondrial dysfunction, could be by-products of environmental stressors such as pollution. There have been reports of autism outbreaks occurring in specific locations.
Since these cases of autism are related to geographic location, the
implication is that something in the environment is complementing an
at-risk genotype
to cause autism in these vulnerable individuals. Mercury and lead both
contribute to inflammation, leading scientists to speculate that these
heavy metals could play a role in autism. These findings are
controversial, however, with many researchers believing that increasing
rates of autism are a consequence of more accurate screening and
diagnostic methods, and are not due to any sort of environmental factor.
Accelerated neural aging
Neuroinflammation is associated with increased rates of neurodegeneration.
Inflammation tends to increase naturally with age. By facilitating
inflammation, pollutants such as air particulates and heavy metals cause
the CNS to age more quickly. Many late-onset diseases are caused by
neurodegeneration. Multiple sclerosis, Parkinson's disease, amyotrophic lateral sclerosis (ALS), and Alzheimer's disease
are all believed to be exacerbated by inflammatory processes, resulting
in individuals displaying signs of these diseases at an earlier age
than is typically expected.
Multiple sclerosis occurs when chronic inflammation leads to the compromise of oligodendrocytes, which in turn leads to the destruction of the myelin sheath. Then axons
begin exhibiting signs of damage, which in turn leads to neuron death.
Multiple sclerosis has been correlated to living in areas with high
particulate matter levels in the air.
In Parkinson's disease, inflammation leading to depletion of antioxidant stores will ultimately lead to dopaminergic
neuron degeneration, causing a shortage of dopamine and contributing to
the formation of Parkinson's disease. Chronic glial activation as a
result of inflammation causes motor neuron death and compromises astrocytes, these factors leading to the symptoms of amyotrophic lateral sclerosis (ALS, aka Lou Gehrig's disease).
In the case of Alzheimer's disease, inflammatory processes lead
to neuron death by inhibiting growth at axons and activating astrocytes
that produce proteoglycans. This product can only be deposited in the hippocampus and cortex, indicating that this may be the reason these two areas show the highest levels of degeneration in Alzheimer's disease. Airborne metal particulates have been shown to directly access and affect the brain through olfactory pathways, which allows a large amount of particulate matter to reach the blood–brain barrier.
These facts, coupled with air pollution's link to neurofibrillary
tangles and the observed subcortical vascular changes observed in dogs,
imply that the negative neuroplastic effects of pollution could result
in increased risk for Alzheimer's disease, and could also implicate
pollution as a cause of early-onset Alzheimer's disease through multiple
mechanisms. The general effect of pollution is increased levels of
inflammation. As a result, pollution can significantly contribute to
various neurological disorders that are caused by inflammatory
processes.
Neuroplasticity, also known as neural plasticity, or brain plasticity, is the ability of neural networks in the brain to change through growth and reorganization. These changes range from individual neuron pathways making new connections, to systematic adjustments like cortical remapping. Examples of neuroplasticity include circuit and network changes that result from learning a new ability, environmental influences, practice, and psychological stress.
Neuroplasticity was once thought by neuroscientists to manifest only during childhood,
but research in the latter half of the 20th century showed that many
aspects of the brain can be altered (or are "plastic") even through
adulthood. However, the developing brain exhibits a higher degree of plasticity than the adult brain. Activity-dependent plasticity can have significant implications for healthy development, learning, memory, and recovery from brain damage.
History
Origin
The term "plasticity" was first applied to behavior in 1890 by William James in The Principles of Psychology. The first person to use the term neural plasticity appears to have been the Polish neuroscientist Jerzy Konorski.
In 1793, Italian anatomist Michele Vicenzo Malacarne described
experiments in which he paired animals, trained one of the pair
extensively for years, and then dissected both. He discovered that the
cerebellums of the trained animals were substantially larger. But these
findings were eventually forgotten. The idea that the brain and its function are not fixed throughout adulthood was proposed in 1890 by William James in The Principles of Psychology, though the idea was largely neglected.
Until around the 1970s, neuroscientists believed that the brain's
structure and function was essentially fixed throughout adulthood.
While the brain was commonly understood as a nonrenewable organ in the early 1900s, Santiago Ramón y Cajal, father of neuroscience, used the term neuronal plasticity to describe nonpathological changes in the structure of adult brains. Based on his renowned Neuron doctrine,
Cajal first described the neuron as the fundamental unit of the nervous
system that later served as an essential foundation to develop the
concept of neural plasticity.
He used the term plasticity in reference to his work on findings of
degeneration and regeneration in the central nervous system after a
person had reached adulthood, specifically. Many neuroscientists used
the term plasticity only to explain the regenerative capacity of the
peripheral nervous system, which Cajal's conceptual transfer of the term
gave rise to a controversial discussion.
The term has since been broadly applied:
Given the central importance of
neuroplasticity, an outsider would be forgiven for assuming that it was
well defined and that a basic and universal framework served to direct
current and future hypotheses and experimentation. Sadly, however, this
is not the case. While many neuroscientists use the word neuroplasticity
as an umbrella term it means different things to different researchers
in different subfields ... In brief, a mutually agreed-upon framework
does not appear to exist.
Research and discovery
In 1923, Karl Lashley conducted experiments on rhesus monkeys
that demonstrated changes in neuronal pathways, which he concluded were
evidence of plasticity. Despite this, and other research that suggested
plasticity took place, neuroscientists did not widely accept the idea
of neuroplasticity.
In 1945, Justo Gonzalo concluded from his research on brain dynamics, that, contrary to the activity of the projection areas,
the "central" cortical mass (more or less equidistant from the visual,
tactile and auditive projection areas), would be a "maneuvering mass",
rather unspecific or multisensory, with capacity to increase neural
excitability and re-organize the activity by means of plasticity
properties. He gives as a first example of adaptation, to see upright with reversing glasses in the Stratton experiment,
and specially, several first-hand brain injuries cases in which he
observed dynamic and adaptive properties in their disorders, in
particular in the inverted perception disorder [e.g., see pp 260–62 Vol.
I (1945), p 696 Vol. II (1950)].
He stated that a sensory signal in a projection area would be only an
inverted and constricted outline that would be magnified due to the
increase in recruited cerebral mass, and re-inverted due to some effect
of brain plasticity, in more central areas, following a spiral growth.
Marian Diamond
of the University of California, Berkeley, produced the first
scientific evidence of anatomical brain plasticity, publishing her
research in 1964.
Other significant evidence was produced in the 1960s and after, notably from scientists including Paul Bach-y-Rita, Michael Merzenich along with Jon Kaas, as well as several others.
In the 1960s, Paul Bach-y-Rita
invented a device that was tested on a small number of people, and
involved a person sitting in a chair, embedded in which were nubs that
were made to vibrate in ways that translated images received in a
camera, allowing a form of vision via sensory substitution.
Studies in people recovering from stroke
also provided support for neuroplasticity, as regions of the brain that
remained healthy could sometimes take over, at least in part, functions
that had been destroyed; Shepherd Ivory Franz did work in this area.
Eleanor Maguire documented changes in hippocampal structure associated with acquiring the knowledge of London's layout in local taxi drivers.
A redistribution of grey matter was indicated in London Taxi Drivers
compared to controls. This work on hippocampal plasticity not only
interested scientists, but also engaged the public and media worldwide.
Michael Merzenich
is a neuroscientist who has been one of the pioneers of neuroplasticity
for over three decades. He has made some of "the most ambitious claims
for the field – that brain exercises may be as useful as drugs to treat
diseases as severe as schizophrenia – that plasticity exists from cradle
to the grave, and that radical improvements in cognitive functioning –
how we learn, think, perceive, and remember are possible even in the
elderly." Merzenich's work was affected by a crucial discovery made by David Hubel and Torsten Wiesel
in their work with kittens. The experiment involved sewing one eye shut
and recording the cortical brain maps. Hubel and Wiesel saw that the
portion of the kitten's brain associated with the shut eye was not idle,
as expected. Instead, it processed visual information from the open
eye. It was "…as though the brain didn't want to waste any 'cortical
real estate' and had found a way to rewire itself."
This implied neuroplasticity during the critical period.
However, Merzenich argued that neuroplasticity could occur beyond the
critical period. His first encounter with adult plasticity came when he
was engaged in a postdoctoral study with Clinton Woosley. The experiment
was based on observation of what occurred in the brain when one
peripheral nerve was cut and subsequently regenerated. The two
scientists micromapped the hand maps of monkey brains before and after
cutting a peripheral nerve and sewing the ends together. Afterwards, the
hand map in the brain that they expected to be jumbled was nearly
normal. This was a substantial breakthrough. Merzenich asserted that,
"If the brain map could normalize its structure in response to abnormal
input, the prevailing view that we are born with a hardwired system had
to be wrong. The brain had to be plastic." Merzenich received the 2016 Kavli Prize in Neuroscience "for the discovery of mechanisms that allow experience and neural activity to remodel brain function."
Neurobiology
JT Wall and J Xu have traced the mechanisms underlying neuroplasticity. Re-organization is not cortically emergent, but occurs at every level in the processing hierarchy; this produces the map changes observed in the cerebral cortex.
Types
Christopher
Shaw and Jill McEachern (eds) in "Toward a theory of Neuroplasticity",
state that there is no all-inclusive theory that overarches different
frameworks and systems in the study of neuroplasticity. However,
researchers often describe neuroplasticity as “the ability to make
adaptive changes related to the structure and function of the nervous
system." Correspondingly, two types of neuroplasticity are often discussed: structural neuroplasticity and functional neuroplasticity.
Structural neuroplasticity
Structural
plasticity is often understood as the brain's ability to change its
neuronal connections. New neurons are constantly produced and integrated
into the central nervous system throughout the life span based on this
type of neuroplasticity. Researchers nowadays use multiple
cross-sectional imaging methods (i.e. magnetic resonance imaging (MRI), computerized tomography (CT)) to study the structural alterations of the human brains.
This type of neuroplasticity often studies the effect of various
internal or external stimuli on the brain's anatomical reorganization.
The changes of grey matter
proportion or the synaptic strength in the brain are considered as
examples of structural neuroplasticity. Structural neuroplasticity is
currently investigated more within the field of neuroscience in current
academia.
Functional neuroplasticity
Functional
plasticity refers to brain's ability to alter and adapt the functional
properties of neurons. The changes can occur in response to previous
activity (activity-dependent plasticity) to acquire memory or in response to malfunction or damage of neurons (reactive plasticity)
to compensate a pathological event. In the latter case the functions
from one part of the brain transfer to another part of the brain based
on the demand to produce recovery of behavioral or physiological
processes. Regarding physiological forms of activity-dependent plasticity, those involving synapses are referred to as synaptic plasticity. The strengthening or weakening of synapses that results in an increase or decrease of firing rate of the neurons are called long-term potentiation (LTP) and long-term depression (LTD), respectively, and they are considered as examples of synaptic plasticity that are associated with memory. The cerebellum is a typical structure with combinations of LTP/LTD and redundancy within the circuitry, allowing plasticity at several sites.
More recently it has become clearer that synaptic plasticity can be
complemented by another form of activity-dependent plasticity involving
the intrinsic excitability of neurons, which is referred to as intrinsic plasticity. This, as opposed to homeostatic plasticity does not necessarily maintain the overall activity of a neuron within a network but contributes to encoding memories.
Applications and examples
The adult brain is not entirely "hard-wired" with fixed neuronal circuits.
There are many instances of cortical and subcortical rewiring of
neuronal circuits in response to training as well as in response to
injury. There is evidence that neurogenesis (birth of brain cells) occurs in the adult, mammalian brain—and such changes can persist well into old age. The evidence for neurogenesis is mainly restricted to the hippocampus and olfactory bulb, but current research has revealed that other parts of the brain, including the cerebellum, may be involved as well.
However, the degree of rewiring induced by the integration of new
neurons in the established circuits is not known, and such rewiring may
well be functionally redundant.
There is now ample evidence
for the active, experience-dependent re-organization of the synaptic
networks of the brain involving multiple inter-related structures
including the cerebral cortex. The specific details of how this process
occurs at the molecular and ultrastructural
levels are topics of active neuroscience research. The way experience
can influence the synaptic organization of the brain is also the basis
for a number of theories of brain function including the general theory
of mind and Neural Darwinism.
The concept of neuroplasticity is also central to theories of memory
and learning that are associated with experience-driven alteration of
synaptic structure and function in studies of classical conditioning in invertebrate animal models such as Aplysia.
Treatment of brain damage
A
surprising consequence of neuroplasticity is that the brain activity
associated with a given function can be transferred to a different
location; this can result from normal experience and also occurs in the
process of recovery from brain injury. Neuroplasticity is the
fundamental issue that supports the scientific basis for treatment of acquired brain injury with goal-directed experiential therapeutic programs in the context of rehabilitation approaches to the functional consequences of the injury.
Neuroplasticity is gaining popularity as a theory that, at least
in part, explains improvements in functional outcomes with physical
therapy post-stroke. Rehabilitation techniques that are supported by
evidence which suggest cortical reorganization as the mechanism of
change include constraint-induced movement therapy, functional electrical stimulation, treadmill training with body-weight support, and virtual reality therapy. Robot assisted therapy
is an emerging technique, which is also hypothesized to work by way of
neuroplasticity, though there is currently insufficient evidence to
determine the exact mechanisms of change when using this method.
One group has developed a treatment that includes increased levels of progesterone injections in brain-injured patients. "Administration of progesterone after traumatic brain injury (TBI) and stroke reduces edema, inflammation, and neuronal cell death, and enhances spatial reference memory and sensory-motor recovery."
In a clinical trial, a group of severely injured patients had a 60%
reduction in mortality after three days of progesterone injections. However, a study published in the New England Journal of Medicine
in 2014 detailing the results of a multi-center NIH-funded phase III
clinical trial of 882 patients found that treatment of acute traumatic
brain injury with the hormone progesterone provides no significant
benefit to patients when compared with placebo.
Binocular vision
For decades, researchers assumed that humans had to acquire binocular vision, in particular stereopsis, in early childhood or they would never gain it. In recent years, however, successful improvements in persons with amblyopia, convergence insufficiency or other stereo vision anomalies have become prime examples of neuroplasticity; binocular vision improvements and stereopsis recovery are now active areas of scientific and clinical research.
Phantom limbs
A
diagrammatic explanation of the mirror box. The patient places the
intact limb into one side of the box (in this case the right hand) and
the amputated limb into the other side. Due to the mirror, the patient
sees a reflection of the intact hand where the missing limb would be
(indicated in lower contrast). The patient thus receives artificial
visual feedback that the "resurrected" limb is now moving when they move
the good hand.
In the phenomenon of phantom limb sensation, a person continues to feel pain or sensation within a part of their body that has been amputated. This is strangely common, occurring in 60–80% of amputees. An explanation for this is based on the concept of neuroplasticity, as the cortical maps of the removed limbs are believed to have become engaged with the area around them in the postcentral gyrus.
This results in activity within the surrounding area of the cortex
being misinterpreted by the area of the cortex formerly responsible for
the amputated limb.
The relationship between phantom limb sensation and neuroplasticity is a complex one. In the early 1990s V.S. Ramachandran theorized that phantom limbs were the result of cortical remapping.
However, in 1995 Herta Flor and her colleagues demonstrated that
cortical remapping occurs only in patients who have phantom pain.
Her research showed that phantom limb pain (rather than referred
sensations) was the perceptual correlate of cortical reorganization. This phenomenon is sometimes referred to as maladaptive plasticity.
In 2009, Lorimer Moseley and Peter Brugger carried out an
experiment in which they encouraged arm amputee subjects to use visual
imagery to contort their phantom limbs into impossible
configurations. Four of the seven subjects succeeded in performing
impossible movements of the phantom limb. This experiment suggests that
the subjects had modified the neural representation of their phantom
limbs and generated the motor commands needed to execute impossible
movements in the absence of feedback from the body.
The authors stated that: "In fact, this finding extends our
understanding of the brain's plasticity because it is evidence that
profound changes in the mental representation of the body can be induced
purely by internal brain mechanisms—the brain truly does change
itself."
Individuals who suffer from chronic pain experience prolonged pain at
sites that may have been previously injured, yet are otherwise
currently healthy. This phenomenon is related to neuroplasticity due to a
maladaptive reorganization of the nervous system, both peripherally and
centrally. During the period of tissue damage, noxious stimuli and inflammation cause an elevation of nociceptive input from the periphery to the central nervous system. Prolonged nociception from the periphery then elicits a neuroplastic response at the cortical level to change its somatotopic organization for the painful site, inducing central sensitization. For instance, individuals experiencing complex regional pain syndrome
demonstrate a diminished cortical somatotopic representation of the
hand contralaterally as well as a decreased spacing between the hand and
the mouth. Additionally, chronic pain has been reported to significantly reduce the volume of grey matter in the brain globally, and more specifically at the prefrontal cortex and right thalamus.
However, following treatment, these abnormalities in cortical
reorganization and grey matter volume are resolved, as well as their
symptoms. Similar results have been reported for phantom limb pain, chronic low back pain and carpal tunnel syndrome.
A number of studies have linked meditation practice to differences in cortical thickness or density of gray matter. One of the most well-known studies to demonstrate this was led by Sara Lazar, from Harvard University, in 2000. Richard Davidson, a neuroscientist at the University of Wisconsin, has led experiments in collaboration with the Dalai Lama
on effects of meditation on the brain. His results suggest that
long-term or short-term practice of meditation can lead to different
levels of activities in brain regions associated with effects such as attention, anxiety, depression, fear, anger,
and compassion as well as the ability of the body to heal itself. These
functional changes may be caused by changes in the physical structure
of the brain.
Due to hearing loss, the auditory cortex and other association areas of the brain in deaf and/or hard of hearing people undergo compensatory plasticity.
The auditory cortex is usually reserved for processing auditory
information in hearing people now is redirected to serve other
functions, especially for vision and somatosensation.
Deaf individuals have enhanced peripheral visual attention, better motion change but not color change detection ability in visual tasks, more effective visual search, and faster response time for visual targets
compared to hearing individuals. Altered visual processing in deaf
people is often found to be associated with the repurposing of other
brain areas including primary auditory cortex, posterior parietal association cortex (PPAC), and anterior cingulate cortex (ACC).
A review by Bavelier et al. (2006) summarizes many aspects on the topic
of visual ability comparison between deaf and hearing individuals.
Brain areas that serve a function in auditory processing
repurpose to process somatosensory information in congenitally deaf
people. They have higher sensitivity in detecting frequency change in
vibration above threshold and higher and more widespread activation in auditory cortex under somatosensory stimulation. However, speeded response for somatosensory stimuli is not found in deaf adults.
Cochlear implant
Neuroplasticity
is involved in the development of sensory function. The brain is born
immature and then adapts to sensory inputs after birth. In the auditory
system, congenital hearing loss, a rather frequent inborn condition
affecting 1 of 1000 newborns, has been shown to affect auditory
development, and implantation of a sensory prostheses activating the auditory system has prevented the deficits and induced functional maturation of the auditory system.
Due to a sensitive period for plasticity, there is also a sensitive
period for such intervention within the first 2–4 years of life.
Consequently, in prelingually deaf children, early cochlear implantation, as a rule, allows the children to learn the mother language and acquire acoustic communication.
Blindness
Due to vision loss, the visual cortex
in blind people may undergo cross-modal plasticity, and therefore other
senses may have enhanced abilities. Or the opposite could occur, with
the lack of visual input weakening the development of other sensory
systems. One study suggests that the right posterior middle temporal
gyrus and superior occipital gyrus reveal more activation in the blind than in the sighted people during a sound-moving detection task.
Several studies support the latter idea and found weakened ability in
audio distance evaluation, proprioceptive reproduction, threshold for
visual bisection, and judging minimum audible angle.
Human echolocation
Human echolocation is a learned ability for humans to sense their environment from echoes. This ability is used by some blind people to navigate their environment and sense their surroundings in detail. Studies in 2010 and 2011 using functional magnetic resonance imaging
techniques have shown that parts of the brain associated with visual
processing are adapted for the new skill of echolocation. Studies with
blind patients, for example, suggest that the click-echoes heard by
these patients were processed by brain regions devoted to vision rather
than audition.
Attention deficit hyperactivity disorder
MRI studies of 1713 participants shows that both children and adults with Attention deficit hyperactivity disorder (ADHD) have smaller volumes of the nucleus accumbens, amygdala, caudate, hippocampus, putamen,
and overall cortical and intracranial volume; and have less surface
area and cortical thickness, compared to people without ADHD. Brain volume does not correlate to intelligence, or Intelligence Quotient,(IQ)
People with ADHD exhibit atypical neuroconnectivity. In particular, it
has been hypothesized that ADHD symptomatology may arise from a
deviation from neurotypical synchronization and interaction within and
between these large-scale networks during brain development.
Investigating functional connectivity using the sub-second temporal
resolution of electroencephalography (EEG) instead allows for the
measurement of a wider range of brain oscillatory phenomena, including
transient changes in connectivity during cognition and behavior.
Neuroplasticity is most active in childhood as a part of normal human development, and can also be seen as an especially important mechanism for children in terms of risk and resiliency.
Trauma is considered a great risk as it negatively affects many areas
of the brain and puts a strain on the sympathetic nervous system from
constant activation. Trauma thus alters the brain's connections such
that children who have experienced trauma may be hyper vigilant or
overly aroused. However, a child's brain can cope with these adverse effects through the actions of neuroplasticity.
There are many examples of neuroplasticity in human development.
For example, Justine Ker and Stephen Nelson looked at the effects of
musical training on neuroplasticity, and found that musical training can
contribute to experience dependent structural plasticity. This is when
changes in the brain occur based on experiences that are unique to an
individual. Examples of this are learning multiple languages, playing a
sport, doing theatre, etc. A study done by Hyde in 2009, showed that
changes in the brain of children could be seen in as little as 15 months
of musical training.
Ker and Nelson suggest this degree of plasticity in the brains of
children can "help provide a form of intervention for children... with
developmental disorders and neurological diseases."
In a single lifespan, individuals of an animal species may encounter various changes in brain morphology. Many of these differences are caused by the release of hormones in the brain; others are the product of evolutionary factors or developmental stages. Some changes occur seasonally in species to enhance or generate response behaviors.
Seasonal brain changes
Changing brain behavior and morphology to suit other seasonal behaviors is relatively common in animals. These changes can improve the chances of mating during breeding season. Examples of seasonal brain morphology change can be found within many classes and species.
Within the class Aves, black-capped chickadees experience an increase in the volume of their hippocampus and strength of neural connections to the hippocampus during fall months. These morphological changes within the hippocampus which are related to spatial memory are not limited to birds, as they can also be observed in rodents and amphibians. In songbirds, many song control nuclei in the brain increase in size during mating season. Among birds, changes in brain morphology to influence song patterns, frequency, and volume are common. Gonadotropin-releasing hormone (GnRH) immunoreactivity, or the reception of the hormone, is lowered in European starlings exposed to longer periods of light during the day.
The California sea hare, a gastropod, has more successful inhibition of egg-laying hormones outside of mating season due to increased effectiveness of inhibitors in the brain. Changes to the inhibitory nature of regions of the brain can also be found in humans and other mammals. In the amphibian Bufo japonicus, part of the amygdala is larger before breeding and during hibernation than it is after breeding.
Seasonal brain variation occurs within many mammals. Part of the hypothalamus of the common ewe is more receptive to GnRH during breeding season than at other times of the year. Humans experience a change in the "size of the hypothalamic suprachiasmatic nucleus and vasopressin-immunoreactive neurons within it" during the fall, when these parts are larger. In the spring, both reduce in size.
Traumatic brain injury research
Randy Nudo's group found that if a small stroke
(an infarction) is induced by obstruction of blood flow to a portion of
a monkey's motor cortex, the part of the body that responds by movement
moves when areas adjacent to the damaged brain area are stimulated. In
one study, intracortical microstimulation (ICMS) mapping techniques were
used in nine normal monkeys. Some underwent ischemic-infarction
procedures and the others, ICMS procedures. The monkeys with ischemic
infarctions retained more finger flexion during food retrieval and after
several months this deficit returned to preoperative levels. With respect to the distal forelimb
representation, "postinfarction mapping procedures revealed that
movement representations underwent reorganization throughout the
adjacent, undamaged cortex."
Understanding of interaction between the damaged and undamaged areas
provides a basis for better treatment plans in stroke patients. Current
research includes the tracking of changes that occur in the motor areas
of the cerebral cortex as a result of a stroke. Thus, events that occur
in the reorganization process of the brain can be ascertained. Nudo is
also involved in studying the treatment plans that may enhance recovery
from strokes, such as physiotherapy, pharmacotherapy, and electrical-stimulation therapy.
Jon Kaas, a professor at Vanderbilt University,
has been able to show "how somatosensory area 3b and ventroposterior
(VP) nucleus of the thalamus are affected by longstanding unilateral
dorsal-column lesions at cervical levels in macaque monkeys."
Adult brains have the ability to change as a result of injury but the
extent of the reorganization depends on the extent of the injury. His
recent research focuses on the somatosensory system, which involves a
sense of the body and its movements using many senses. Usually, damage
of the somatosensory cortex results in impairment of the body
perception. Kaas' research project is focused on how these systems
(somatosensory, cognitive, motor systems) respond with plastic changes
resulting from injury.
One recent study of neuroplasticity involves work done by a team of doctors and researchers at Emory University, specifically Dr. Donald Stein
and Dr. David Wright. This is the first treatment in 40 years that has
significant results in treating traumatic brain injuries while also
incurring no known side effects and being cheap to administer.
Dr. Stein noticed that female mice seemed to recover from brain
injuries better than male mice, and that at certain points in the estrus cycle,
females recovered even better. This difference may be attributed to
different levels of progesterone, with higher levels of progesterone
leading to the faster recovery from brain injury in mice. However,
clinical trials showed progesterone offers no significant benefit for
traumatic brain injury in human patients.
Aging
Transcriptional profiling of the frontal cortex of persons ranging from 26 to 106 years of age defined a set of genes with reduced expression after age 40, and especially after age 70. Genes that play central roles in synaptic plasticity
were the most significantly affected by age, generally showing reduced
expression over time. There was also a marked increase in cortical DNA damage, likely oxidative DNA damage, in gene promoters with aging.
Reactive oxygen species appear to have a significant role in the regulation of synaptic plasticity and cognitive function. However age-related increases in reactive oxygen species may also lead to impairments in these functions.
Multilingualism
The
beneficial effect of multilingualism on people's behavior and cognition
is well-known nowadays. Numerous studies have shown that people who
study more than one language have better cognitive functions and
flexibilities than people who only speak one language. Bilinguals are
found to have longer attention spans, stronger organization and
analyzation skills, and a better theory of mind than monolinguals.
Researchers have found that the effect of multilingualism on better
cognition is due to neuroplasticity.
In one prominent study, neurolinguists used a voxel-based morphometry
(VBM) method to visualize the structural plasticity of brains in
healthy monolinguals and bilinguals. They first investigated the
differences in density of grey and white matter between two groups and
found the relationship between brain structure and age of language
acquisition. The results showed that grey-matter density in the inferior
parietal cortex for multilinguals were significantly greater than
monolinguals. The researchers also found that early bilinguals had a
greater density of grey matter relative to late bilinguals in the same
region. The inferior parietal cortex is a brain region highly associated
with the language learning, which corresponds to the VBM result of the
study.
Recent studies have also found that learning multiple languages
not only re-structures the brain but also boosts brain's capacity for
plasticity. A recent study found that multilingualism not only affects
the grey matter but also white matter of the brain. White matter is made up of myelinated axons that is greatly associated with learning and communication. Neurolinguists used a diffusion tensor imaging
(DTI) scanning method to determine the white matter intensity between
monolinguals and bilinguals. Increased myelinations in white matter
tracts were found in bilingual individuals who actively used both
languages in everyday life. The demand of handling more than one
language requires more efficient connectivity within the brain, which
resulted in greater white matter density for multilinguals.
While it is still debated whether these changes in brain are
result of genetic disposition or environmental demands, many evidences
suggest that environmental, social experience in early multilinguals
affect the structural and functional reorganization in the brain.
A
rodent is not stimulated by the environment in a wire cage, and this
affects its brain negatively, particularly the complexity of its
synaptic connections
Environmental enrichment is the stimulation of the brain by its physical and social surroundings. Brains in richer, more stimulating environments have higher rates of synaptogenesis and more complex dendrite arbors, leading to increased brain activity. This effect takes place primarily during neurodevelopment, but also during adulthood to a lesser degree. With extra synapses there is also increased synapse activity, leading to an increased size and number of glial energy-support cells. Environmental enrichment also enhances capillary vasculation, providing the neurons and glial cells with extra energy. The neuropil
(neurons, glial cells, capillaries, combined) expands, thickening the
cortex. Research on rodent brains suggests that environmental enrichment
may also lead to an increased rate of neurogenesis.
Research on animals finds that environmental enrichment could aid
the treatment and recovery of numerous brain-related dysfunctions,
including Alzheimer's disease and those connected to aging,
whereas a lack of stimulation might impair cognitive development.
Moreover, this research also suggests that environmental enrichment
leads to a greater level of cognitive reserve, the brain's resilience to the effects of conditions such as aging and dementia.
Research on humans suggests that lack of stimulation delays and
impairs cognitive development. Research also finds that attaining and
engaging in higher levels of education, environments in which people
participate in more challenging cognitively stimulating activities,
results in greater cognitive reserve.
Early research
Donald O. Hebb in 1947 found that rats raised as pets performed better on problem solving tests than rats raised in cages.
His research, however, did not investigate the brain nor use
standardized impoverished and enriched environments. Research doing this
first was started in 1960 at the University of California, Berkeley by Mark Rosenzweig,
who compared single rats in normal cages, and those placed in ones with
toys, ladders, tunnels, running wheels in groups. This found that
growing up in enriched environments affected enzyme cholinesterase activity. This work led in 1962 to the discovery that environmental enrichment increased cerebral cortex volume. In 1964, it was found that this was due to increased cerebral cortex thickness and greater synapse and glial numbers.
Also starting around 1960, Harry Harlow studied the effects of maternal and social deprivation on rhesus monkey infants (a form of environmental stimulus deprivation). This established the importance of social stimulation for normal cognitive and emotional development.
Synapses
Synaptogenesis
Rats raised with environmental enrichment have thicker cerebral cortices (3.3–7%) that contain 25% more synapses. This effect of environmental richness upon the brain occurs whether it is experienced immediately following birth, after weaning, or during maturity.
When synapse numbers increase in adults, they can remain high in number
even when the adults are returned to impoverished environment for 30
days
suggesting that such increases in synapse numbers are not necessarily
temporary. However, the increase in synapse numbers has been observed
generally to reduce with maturation. Stimulation affects not only synapses upon pyramidal neurons (the main projecting neurons in the cerebral cortex) but also stellate ones (that are usually interneurons). It can also affect neurons outside the brain, such as those in the retina.
Dendrite complexity
Environmental enrichment affects the complexity and length of the dendrite arbors (upon which synapses form). Higher-order dendrite branch complexity is increased in enriched environments, as can the length, in young animals, of distal branches. Environmental enrichment rescues harmful effects of stress on dendritic complexity.
Activity and energy consumption
Animals in enriched environments show evidence of increased synapse activation. Synapses tend to also be much larger. Gamma oscillations become larger in amplitude in the hippocampus.
This increased energy consumption is reflected in glial and local
capillary vasculation that provides synapses with extra energy.
Glial cell numbers per neuron increase 12–14%
The direct apposition area of glial cells with synapses expands by 19%
The volume of glial cell nuclei for each synapse is higher by 37.5%
The mean volume of mitochondria per neuron is 20% greater
The volume of glial cell nuclei for each neuron is 63% higher
Capillary density is increased.
Capillaries are wider (4.35 μm compared to 4.15 μm in controls)
Shorter distance exist between any part of the neuropil and a capillary (27.6 μm compared to 34.6 μm)
These energy related changes to the neuropil
are responsible for increasing the volume of the cerebral cortex (the
increase in synapse numbers contributes in itself hardly any extra
volume).
Motor learning stimulation
Part of the effect of environmental enrichment is providing opportunities to acquire motor skills. Research on rats learning an “acrobatic” skill shows that such learning activity leads to increased synapse count.
Maternal transmission
Environmental enrichment during pregnancy has effects upon the fetus, such as accelerating his or her retinal development.
Neurogenesis
Environmental enrichment can also lead to the formation of neurons (at least in rats) and reverse both the loss of neurons in the hippocampus and memory impairment from chronic stress. However, its relevance has been questioned for the behavioral effects of enriched environments.
Mechanisms
Enriched environments affect the expression of genes that determine neuronal structure in the cerebral cortex and hippocampus. At the molecular level, this occurs through increased concentrations of the neurotrophinsNGF, NT-3, and changes in BDNF. This alters the activation of cholinergic neurons, 5-HT, and beta-adrenolin. Another effect is to increase proteins such as synaptophysin and PSD-95 in synapses. Changes in Wnt signaling have also been found to mimic in adult mice the effects of environmental enrichment upon synapses in the hippocampus. Increase in neurons numbers could be linked to changes in VEGF.
Rehabilitation and resilience
Research
in animals suggests that environmental enrichment aids recovery from
certain neurological disorders and cognitive impairments. There are two
mains areas of focus: neurological rehabilitation and cognitive reserve,
the brain's resistance to the effects of exposure to physical, natural,
and social threats. Although most of these experiments used animal
subjects, mainly rodents, researchers have pointed to the affected areas
of animal brains to which human brains are most similar and used their
findings as evidence to show that humans would have comparable reactions
to enriched environments. The tests done on animals are thus meant to
represent human simulations for the following list of conditions.
Neurological rehabilitation
Autism
A
study conducted in 2011 led to the conclusion that environmental
enrichment vastly improves the cognitive ability of children with autism. The study found that autistic children who receive olfactory and tactile stimulation along with exercises
that stimulated other paired sensory modalities clinically improved by
42 percent while autistic children not receiving this treatment
clinically improved by just 7 percent.
The same study also showed that there was significant clinical
improvement in autistic children exposed to enriched sensorimotor
environments, and a vast majority of parents reported that their child's
quality of life was much better with the treatment.
A second study confirmed its effectiveness. The second study also
found after 6 months of sensory enrichment therapy, 21% of the children
who initially had been given an autism classification, using the Autism
Diagnostic Observation Schedule, improved to the point that, although
they remained on the autism spectrum, they no longer met the criteria
for classic autism. None of the standard care controls reached an
equivalent level of improvement. The therapy using the methodologies is titled Sensory Enrichment Therapy.
Alzheimer's disease
Through
environmental enrichment, researchers were able to enhance and
partially repair memory deficits in mice between ages of 2 to 7 months
with characteristics of Alzheimer's disease. Mice in enriched environments performed significantly better on object recognition tests and the Morris Water Maze
than they had when they were in standard environments. It was thus
concluded that environmental enrichment enhances visual and learning
memory for those with Alzheimer's.
Furthermore, it has been found that mouse models of Alzheimer's disease
that were exposed to enriched environment before amyloid onset (at 3
months of age) and then returned to their home cage for over 7 months,
showed preserved spatial memory and reduced amyloid deposition at 13
months old, when they are supposed to show dramatic memory deficits and
amyloid plaque load. These findings reveal the preventive, and
long-lasting effects of early life stimulating experience on
Alzheimer-like pathology in mice and likely reflect the capacity of
enriched environment to efficiently stimulate the cognitive reserve.
Huntington's disease
Research has indicated that environmental enrichment can help relieve motor and psychiatric deficits caused by Huntington's disease. It also improves lost protein levels for those with the disease, and prevents striatal and hippocampal deficits in the BDNF, located in the hippocampus.
These findings have led researchers to suggest that environmental
enrichment has a potential to be a possible form of therapy for those
with Huntington's.
Parkinson's disease
Multiple
studies have reported that environmental enrichment for adult mice
helps relieve neuronal death, which is particularly beneficial to those
with Parkinson's disease. A more recent study shows that environmental enrichment particularly affects the nigrostriatal pathway, which is important for managing dopamine and acetylcholine levels, critical for motor deficits.
Moreover, it was found that environmental enrichment has beneficial
effects for the social implications of Parkinson's disease.
Stroke
Research done in animals has shown that subjects recovering in an enriched environment 15 days after having a stroke
had significantly improved neurobehavioral function. In addition these
same subjects showed greater capability of learning and larger infarct
post-intervention than those who were not in an enriched environment. It
was thus concluded that environmental enrichment had a considerable
beneficial effect on the learning and sensorimotor functions on animals
post-stroke.
A 2013 study also found that environmental enrichment socially benefits
patients recovering from stroke. Researchers in that study concluded
that stroke patients in enriched environments in assisted-care
facilities are much more likely to be engaging with other patients
during normal social hours instead of being alone or sleeping.
Rett syndrome
A
2008 study found that environmental enrichment was significant in
aiding recovery of motor coordination and some recovery of BDNF levels
in female mice with conditions similar to those of Rett syndrome.
Over the course of 30 weeks female mice in enriched environments showed
superior ability in motor coordination to those in standard conditions.
Although they were unable to have full motor capability, they were able
to prevent a more severe motor deficit by living in an enriched
environment. These results combined with increased levels of BDNF in the
cerebellum led researchers to conclude that an enriched environment
that stimulates areas of the motor cortex and areas of the cerebellum
having to do with motor learning is beneficial in aiding mice with Rett
syndrome.
Amblyopia
A recent study found that adult rats with amblyopia improved visual acuity two weeks after being placed into an enriched environment.
The same study showed that another two weeks after ending environmental
enrichment, the rats retained their visual acuity improvement.
Conversely, rats in a standard environment showed no improvement in
visual acuity. It was thus concluded that environmental enrichment
reduces GABA inhibition and increases BDNF expression in the visual
cortex. As a result, the growth and development of neurons and synapses
in the visual cortex were much improved due to the enriched environment.
Sensory deprivation
Studies have shown that with the help of environmental enrichment the effects of sensory deprivation
can be corrected. For example, a visual impairment known as
"dark-rearing" in the visual cortex can be prevented and rehabilitated.
In general, an enriched environment will improve, if not repair, the
sensory systems animals possess.
Lead poisoning
During development, gestation
is one of the most critical periods for exposure to any lead. Exposure
to high levels of lead at this time can lead to inferior spatial
learning performance. Studies have shown that environmental enrichment
can overturn damage to the hippocampus induced by lead exposure.
Learning and spatial memory that are dependent on the long-term
potentiation of the hippocampus are vastly improve as subjects in an
enriched environments had lower levels of lead concentration in their
hippocampi. The findings also showed that enriched environments result
in some natural protection of lead-induced brain deficits.
Chronic spinal cord injuries
Research has indicated that animals suffering from spinal cord injuries
showed significant improvement in motor capabilities even with a long
delay in treatment after the injury when exposed to environmental
enrichment.
Social interactions, exercise, and novelty all play major roles in
aiding the recovery of an injured subject. This has led to some
suggestions that the spinal cord has a continued plasticity and all
efforts must be made for enriched environments to stimulate this
plasticity in order to aid recovery.
Maternal deprivation stress
Maternal deprivation
can be caused by the abandonment by a nurturing parent at a young age.
In rodents or nonhuman primates, this leads to a higher vulnerability
for
stress-related illness.
Research suggests that environmental enrichment can reverse the effects
of maternal separation on stress reactivity, possibly by affecting the
hippocampus, the amygdala and the prefrontal cortex.
Child neglect
In
all children, maternal care is one of the significant influences for
hippocampal development, providing the foundation for stable and
individualized learning and memory. However, this is not the case for
those who have experienced child neglect.
Researchers determined that through environmental enrichment, a
neglected child can partially receive the same hippocampal development
and stability, albeit not at the same level as that of the presence of a
parent or guardian.
The results were comparable to those of child intervention programs,
rendering environmental enrichment a useful method for dealing with
child neglect.
Cognitive reserve
Aging
Decreased hippocampal neurogenesis is a characteristic of aging.
Environmental enrichment increases neurogenesis in aged rodents by
potentiating neuronal differentiation and new cell survival.
As a result, subjects exposed to environmental enrichment aged better
due to superior ability in retaining their levels of spatial and
learning memory.
Prenatal and perinatal cocaine exposure
Research has shown that mice exposed to environmental enrichment are less affected by the consequences of cocaine exposure
in comparison with those in standard environments. Although the levels
of dopamine in the brains of both sets of mice were relatively similar,
when both subjects were exposed to the cocaine injection, mice in
enriched environment were significantly less responsive than those in
standard environments.
It was thus concluded that both the activating and rewarding effects
are suppressed by environmental enrichment and early exposure to
environmental enrichment can help prevent drug addiction.
Humans
Though environmental enrichment research has been mostly done upon rodents, similar effects occur in primates,
and are likely to affect the human brain. However, direct research upon
human synapses and their numbers is limited since this requires histological
study of the brain. A link, however, has been found between educational
level and greater dendritic branch complexity following autopsy removal
of the brain.
Localized cerebral cortex changes
MRI detects localized cerebral cortex expansion after people learn complex tasks such as mirror reading (in this case in the right occipital cortex), three-ball juggling (bilateral mid-temporal area and left posterior intraparietal sulcus), and when medical students intensively revise for exams (bilaterally in the posterior and lateral parietal cortex).
Such changes in gray matter volume can be expected to link to changes
in synapse numbers due to the increased numbers of glial cells and the
expanded capillary vascularization needed to support their increased
energy consumption.
Institutional deprivation
Children
that receive impoverished stimulation due to being confined to cots
without social interaction or reliable caretakers in low quality orphanages show severe delays in cognitive and social development. 12% of them if adopted after 6 months of age show autistic or mildly autistic traits later at four years of age.
Some children in such impoverished orphanages at two and half years of
age still fail to produce intelligible words, though a year of foster
care enabled such children to catch up in their language in most
respects.
Catch-up in other cognitive functioning also occurs after adoption,
though problems continue in many children if this happens after the age
of 6 months.
Such children show marked differences in their brains, consistent
with research upon experiment animals, compared to children from
normally stimulating environments. They have reduced brain activity in
the orbital prefrontal cortex, amygdala, hippocampus, temporal cortex, and brain stem. They also showed less developed white matter connections between different areas in their cerebral cortices, particularly the uncinate fasciculus.
Conversely, enriching the experience of preterm infants with massage quickens the maturating of their electroencephalographic activity and their visual acuity. Moreover, as with enrichment in experimental animals, this associates with an increase in IGF-1.
Cognitive reserve and resilience
Another source of evidence for the effect of environment stimulation upon the human brain is cognitive reserve
(a measure of the brain's resilience to cognitive impairment) and the
level of a person's education. Not only is higher education linked to a
more cognitively demanding educational experience, but it also
correlates with a person's general engagement in cognitively demanding
activities. The more education a person has received, the less the effects of aging, dementia, white matter hyperintensities, MRI-defined brain infarcts, Alzheimer's disease, and traumatic brain injury. Also, aging and dementia are less in those that engage in complex cognitive tasks. The cognitive decline of those with epilepsy could also be affected by the level of a person's education.
