Malleability of intelligence

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Malleability of intelligence describes the processes by which intelligence can increase or decrease over time and is not static. These changes may come as a result of genetics, pharmacological factors, psychological factors, behavior, or environmental conditions. Malleable intelligence may refer to changes in cognitive skills, memory, reasoning, or muscle memory related motor skills. In general, the majority of changes in human intelligence occur at either the onset of development, during the critical period, or during old age (see neuroplasticity).

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Charles Spearman, who coined the general intelligence factor "g", described intelligence as one's ability to adapt to his environment with a set of useful skills including reasoning and understanding patterns and relationships. He believed individuals highly developed in one intellectual ability tended to be highly developed at other intellectual abilities. A more intelligent individual was thought to be able to more easily "accommodate" experiences into existing cognitive structures to develop structures more compatible with environmental stimuli. [1]

In general, intelligence is thought to be attributed to both genetic and environmental factors, but the extent to which each plays a key role is highly disputed. Studies of identical and non-identical twins raised separately and together show a strong correlation between child IQ and socio-economic level of the parents. Children raised in lower-class families tend to score lower on intelligence tests when compared to children raised in both middle and upper-class families. However, there is no difference in intelligence scores between children raised in middle versus upper-class families. [2]

Definitions

Neuroscience basis

The biological basis of intelligence is founded in the degree of connectivity of neurons in the brain and the varying amounts of white and grey matter. Studies show that intelligence is positively correlated with total cerebral volume. [1] While it is true that the number of neurons in the brain actually decreases throughout development, as neural connections grow and the pathways become more efficient, the supporting structures in the brain increase. This increase in supporting tissues, which include myelination, blood vessels, and glial cells, leads to an increase in overall brain size. [1] When brain circumference and IQ were compared in 9 year olds, a positive correlation was found between the two. An increase of 2.87 IQ points occurred for each standard deviation increase in brain circumference. [5]

Importance of critical period

The brain grows rapidly for the first five years of human development. At age five, the human brain is 90% of its total size. Then the brain finishes growing gradually until mid to late twenties. From start to finish, the brain increases in size by over 300% from birth. [2] The critical period, defined as the beginning years of brain development, is essential to intellectual development, as the brain optimizes the overproduction of synapses present at birth. [2] During the critical period, the neuronal pathways are refined based on which synapses are active and receiving transmission. It is a "use it or lose it" phenomenon. [2]

Neural plasticity

Neural plasticity refers to any change in the structure of the neural network that forms the central nervous system. Neural plasticity is the neuronal basis for changes in how the mind works, including learning, the formation of memory, and changes in intelligence. One well-studied form of plasticity is Long-Term Potentiation (LTP). [6] It refers to a change in neural connectivity as a result of high activation on both sides of a synaptic cleft. This change in neural connectivity allows information to be more easily processed, as the neural connection associated with that information becomes stronger through LTP. [2] Other forms of plasticity involve the growth of new neurons, the growth of new connections between neurons, and the selective elimination of such connection, called "dendritic pruning". [7]

Genetic factors of intelligence

Humans have varying degrees of neuroplasticity due to their genetic makeups, which affects their ability to adapt to conditions in their environments and effectively learn from experiences. [1] The degree to which intelligence test scores can be linked to genetic heritability increases with age. There is presently no explanation for this puzzling result, but flaws in the testing methods are suspected. A study of Dutch twins concludes that intelligence of 5 year olds is 26% heritable, while the test scores of 12-year-olds is 64% heritable. Structurally, genetic influences explain 77–88% of the variance in the thickness of the mid-sagittal area of the corpus callosum, the volume of the caudate nucleus, and the volumes of the parietal and temporal lobes. [3]

Pharmacological influence

Numerous pharmacological developments have been made to help organize neural circuitry for patients with learning disorders. The cholinergic and glutamatergic systems in the brain serve an important role in learning, memory, and the developmental organization of neuronal circuitry. These systems help to capitalize on the critical period and organize synaptic transmission. Autism and other learning disabilities have been targeted with drugs focusing on cholinergic and glutamatergic transmission. These drugs increase the amount of acetylcholine present in the brain by increasing the production of acetylcholine precursors, as well as inhibiting acetylcholine degradation by cholinesterases. By focusing on heightening the activity of this system, the brain's responsiveness to activity-dependent plasticity is improved. Specifically, glutamatergic drugs may reduce the threshold for LTP, promote more normal dendritic spine morphology, and retain a greater number of useful synaptic connections. Cholinergic drugs may reconnect the basal forebrain with the cortex and hippocampus, connections that are often disrupted in patients with learning disorders. [8]

Psychological factors

Psychological factors and preconceived notions about intelligence can be as influential on intelligence as genetic makeup. Children with early chronic stress show impaired corticolimbic connectivity in development. Early chronic stress is defined as inconsistent or inadequate care-giving and disruption to early rearing environment. These children showed decreased cognitive function, especially in fluid cognition, or the ability to effectively utilize working memory. The lack of connectivity between the limbic system and the prefrontal cortex can be blamed for this deficiency. [9]

Behavioral factors

In the study of malleable intelligence, behavioral factors are often the most intriguing because these are factors humans can seek to control. There are numerous behavioral factors that affect intellectual development and neural plasticity. The key is plasticity, which is caused by experience-driven electrical activation of neurons. This experience-driven activation causes axons to sprout new branches and develop new presynaptic terminals. [2] These new branches often lead to greater mental processing in different areas.

Taking advantage of the critical period

As previously discussed, the critical period is a time of neural pruning and great intellectual development. [2]

See also

Related Research Articles

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The following outline is provided as an overview of and topical guide to neuroscience:

<span class="mw-page-title-main">Cholinergic</span> Agent which mimics choline

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<span class="mw-page-title-main">Nucleus accumbens</span> Region of the basal forebrain

The nucleus accumbens is a region in the basal forebrain rostral to the preoptic area of the hypothalamus. The nucleus accumbens and the olfactory tubercle collectively form the ventral striatum. The ventral striatum and dorsal striatum collectively form the striatum, which is the main component of the basal ganglia. The dopaminergic neurons of the mesolimbic pathway project onto the GABAergic medium spiny neurons of the nucleus accumbens and olfactory tubercle. Each cerebral hemisphere has its own nucleus accumbens, which can be divided into two structures: the nucleus accumbens core and the nucleus accumbens shell. These substructures have different morphology and functions.

<span class="mw-page-title-main">Brain-derived neurotrophic factor</span> Protein

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<span class="mw-page-title-main">Dopaminergic pathways</span> Projection neurons in the brain that synthesize and release dopamine

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Neuroplasticity, also known as neural plasticity, or brain plasticity, is the ability of neural networks in the brain to change through growth and reorganization. It is when the brain is rewired to function in some way that differs from how it previously functioned. 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.

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<span class="mw-page-title-main">Basal forebrain</span> Brain structures in the forebrain

Part of the human brain, the basal forebrain structures are located in the forebrain to the front of and below the striatum. They include the ventral basal ganglia, nucleus basalis, diagonal band of Broca, substantia innominata, and the medial septal nucleus. These structures are important in the production of acetylcholine, which is then distributed widely throughout the brain. The basal forebrain is considered to be the major cholinergic output of the central nervous system (CNS) centred on the output of the nucleus basalis. The presence of non-cholinergic neurons projecting to the cortex have been found to act with the cholinergic neurons to dynamically modulate activity in the cortex.

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<span class="mw-page-title-main">Nonsynaptic plasticity</span> Form of neuroplasticity

Nonsynaptic plasticity is a form of neuroplasticity that involves modification of ion channel function in the axon, dendrites, and cell body that results in specific changes in the integration of excitatory postsynaptic potentials and inhibitory postsynaptic potentials. Nonsynaptic plasticity is a modification of the intrinsic excitability of the neuron. It interacts with synaptic plasticity, but it is considered a separate entity from synaptic plasticity. Intrinsic modification of the electrical properties of neurons plays a role in many aspects of plasticity from homeostatic plasticity to learning and memory itself. Nonsynaptic plasticity affects synaptic integration, subthreshold propagation, spike generation, and other fundamental mechanisms of neurons at the cellular level. These individual neuronal alterations can result in changes in higher brain function, especially learning and memory. However, as an emerging field in neuroscience, much of the knowledge about nonsynaptic plasticity is uncertain and still requires further investigation to better define its role in brain function and behavior.

Developmental plasticity is a general term referring to changes in neural connections during development as a result of environmental interactions as well as neural changes induced by learning. Much like neuroplasticity, or brain plasticity, developmental plasticity is specific to the change in neurons and synaptic connections as a consequence of developmental processes. A child creates most of these connections from birth to early childhood. There are three primary methods by which this may occur as the brain develops, but critical periods determine when lasting changes may form. Developmental plasticity may also be used in place of the term phenotypic plasticity when an organism in an embryonic or larval stage can alter its phenotype based on environmental factors. However, a main difference between the two is that phenotypic plasticity experienced during adulthood can be reversible, whereas traits that are considered developmentally plastic set foundations during early development that remain throughout the life of the organism.

Memory allocation is a process that determines which specific synapses and neurons in a neural network will store a given memory. Although multiple neurons can receive a stimulus, only a subset of the neurons will induce the necessary plasticity for memory encoding. The selection of this subset of neurons is termed neuronal allocation. Similarly, multiple synapses can be activated by a given set of inputs, but specific mechanisms determine which synapses actually go on to encode the memory, and this process is referred to as synaptic allocation. Memory allocation was first discovered in the lateral amygdala by Sheena Josselyn and colleagues in Alcino J. Silva's laboratory.

<span class="mw-page-title-main">Cholinergic neuron</span> Type of nerve cell

A cholinergic neuron is a nerve cell which mainly uses the neurotransmitter acetylcholine (ACh) to send its messages. Many neurological systems are cholinergic. Cholinergic neurons provide the primary source of acetylcholine to the cerebral cortex, and promote cortical activation during both wakefulness and rapid eye movement sleep. The cholinergic system of neurons has been a main focus of research in aging and neural degradation, specifically as it relates to Alzheimer's disease. The dysfunction and loss of basal forebrain cholinergic neurons and their cortical projections are among the earliest pathological events in Alzheimer's disease.

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