Intellectual Disability

Abstract

Intellectual disability is a neurodevelopmental condition defined by significant limitations in *both* intellectual functioning — reasoning, problem-solving, and learning — *and* adaptive behaviour, the everyday skills people use to function, with onset during the developmental period. Its interest for cognitive psychology is that it is the boundary case against which theories of intelligence, memory, and executive control are tested: a condition affecting roughly 1% of the population in which a shortfall in general ability is inseparable from a shortfall in real-world competence. This article sets out the two-part definition and how the AAIDD, DSM-5, and ICD-11 operationalise it, the working-memory and executive weaknesses that accompany it, its heterogeneous aetiology — from the polygenic tail of the normal distribution to discrete causes such as Down syndrome and Williams syndrome — and what it reveals about the typical mind.

Keywords: adaptive behaviour, intellectual functioning, developmental period, neurodevelopmental disorder, aetiological heterogeneity

Intellectual disability occupies a peculiar and important place in cognitive psychology. Most of the field studies specific faculties — attention, working memory, language — in isolation, but intellectual disability is defined at the level of *general* ability, the very construct that theories of intelligence try to explain. It is also the condition where the abstraction of a test score meets the concreteness of a life: the diagnosis has never rested on a low IQ alone, but on the conjunction of below-average intellectual functioning with genuine limitations in *adaptive behaviour* — whether a person can manage money, follow social rules, and look after themselves (Tasse et al., 2012). That two-part structure is why the condition matters here: it forces a distinction, easy to blur in the laboratory, between what a mind can do on a test and what it can do in the world.

The account below moves from what intellectual disability is and how it is classified, through its direct genetic subtypes, the two-part diagnostic definition and the cognitive profile that underlies it, to its heterogeneous aetiology, the way severity is graded, and development across the lifespan. The recurring theme is that intellectual disability is not one thing but a final common pathway reached by hundreds of distinct causes — and that its very generality makes it a uniquely revealing test of how the components of cognition combine into the everyday competence we call intelligence.

What Intellectual Disability Is

Intellectual disability is a condition, arising during the developmental period, that is characterised by significant limitations in both intellectual functioning and adaptive behaviour. *Intellectual functioning* refers to general mental capacity — reasoning, planning, problem-solving, abstract thinking, and learning — the construct that intelligence tests are designed to estimate, conventionally summarised as an IQ. *Adaptive behaviour* refers to the conceptual, social, and practical skills that people learn and use in everyday life. The modern definition, developed over decades by the American Association on Intellectual and Developmental Disabilities (AAIDD) and mirrored in the DSM-5 and ICD-11, insists on all three elements together: neither a low test score by itself nor everyday difficulty by itself is sufficient (Tasse et al., 2012). This is the single most important point for understanding the condition cognitively, because it locates intellectual disability not in a number but in the relationship between measured ability and real-world competence.

The term itself is recent. What is now called intellectual disability was for most of the twentieth century known by a clinical label since superseded, and earlier still by a series of terms now regarded as offensive. The shift in name accompanied a shift in concept: away from a fixed defect residing in the person and toward a description of the *fit* between an individual's capacities and the demands of their environment, with the level of needed support — rather than the deficit alone — increasingly central to how the condition is framed (Schalock et al., 2010). The ICD-11 went further, renaming the category *disorders of intellectual development* to emphasise the developmental and neurobiological basis of the condition (Salvador-Carulla et al., 2011).

Because the defining limitations must arise during the developmental period — conventionally before adulthood — intellectual disability is distinguished from conditions such as dementia, in which comparable cognitive limitations appear after a period of typical functioning. This developmental criterion is not a technicality: it marks intellectual disability as a condition of how the mind is *built*, rather than of how an already-built mind later declines, and it is one reason the condition is so informative about the ordinary course of cognitive development (Patel, Cabral, Ho, & Merrick, 2020).

Types of Intellectual Disability

In the Medical Subject Headings (MeSH) vocabulary maintained by the US National Library of Medicine, Intellectual Disability sits beneath the broader heading Neurobehavioral Manifestations (and, in a second branch, Neurodevelopmental Disorders), and it has a set of direct subtypes: specific, mostly genetic, syndromes in which intellectual disability is a defining feature. It is worth stressing that this list is a *classification for indexing the literature*, not a cognitive taxonomy. The subtypes below are named syndromes with identified causes; they are only a fraction of the hundreds of conditions that can produce intellectual disability, and they cut across the *severity* grading (mild to profound) and the *aetiological* distinctions (syndromic versus non-syndromic) discussed later, which are orthogonal ways of carving up the same territory. A given person's intellectual disability is described by all of these axes at once — a named cause, a severity level, and an adaptive-behaviour profile.

Core Features

The cognitive core of intellectual disability is not a single deficit but the conjunction of two: a general limitation in intellectual functioning and a corresponding limitation in adaptive behaviour. *Intellectual functioning* is operationalised through individually administered intelligence tests, and the conventional threshold is a score of roughly two standard deviations below the population mean — on the usual scale, an IQ of about 70, allowing for the standard error of measurement, so a band of roughly 65 to 75 rather than a hard line (American Psychiatric Association, 2013). But the framework has always resisted treating this number as the diagnosis. A person whose measured functioning is low but who meets the ordinary demands of daily life is not, on the modern definition, intellectually disabled; the test score is a clue, not a verdict (Tasse et al., 2012).

*Adaptive behaviour* is the second, co-equal criterion, and its careful conceptualisation is one of the field's central contributions. It is understood as a set of skills organised into three domains: the *conceptual* (language, reading and writing, money, time, and number concepts), the *social* (interpersonal skills, social responsibility, self-esteem, gullibility, following rules, and avoiding victimisation), and the *practical* (activities of daily living, occupational skills, health care, travel, and use of the telephone). Significant limitation in *at least one* of these domains, measured against normed scales and everyday performance rather than best possible capability, is required for diagnosis (Tasse et al., 2012). The insistence that adaptive behaviour be assessed as *typical* performance in real settings, not as what a person could manage under ideal test conditions, is what keeps the construct tied to the reality of a life.

The relationship between the two criteria is the source of much of the condition's conceptual subtlety. Intellectual functioning and adaptive behaviour are correlated but far from identical: two people with the same IQ can differ widely in how well they cope, because coping draws on motivation, opportunity, support, and specific skills that a global ability score does not capture. This is why the AAIDD framework foregrounds the *supports* a person needs to participate rather than the deficit alone, and why the same underlying limitation can be more or less disabling depending on the demands and accommodations of the environment (Schalock et al., 2010).

Aetiology and Mechanisms

Intellectual disability is best understood not as a disease but as a *final common pathway* reached by an enormous number of distinct causes — genetic, metabolic, infectious, traumatic, and environmental. A useful organising idea, dating to the mid-twentieth century, is the *two-group approach*: the observation that the population of people with intellectual disability seems to comprise two overlapping subpopulations. One, associated with milder impairment, grades smoothly into the lower tail of the normal distribution of ability and reflects the same polygenic and environmental influences that produce individual differences in intelligence throughout the population. The other, associated with more severe impairment, reflects discrete *pathological* causes — single-gene mutations, chromosomal anomalies, and brain insults — that would not have occurred by the ordinary variation of a normal distribution (Reichenberg et al., 2016).

This two-group idea has received striking modern support. A large population study found genuine *discontinuity* in the causes of the intellectual-disability spectrum: mild intellectual disability was strongly familial and behaved like the extreme of a continuous, heritable trait, whereas severe intellectual disability showed weak familial aggregation and was better explained by de novo, non-inherited events — exactly the pattern the two-group model predicts (Reichenberg et al., 2016). The severe end, in other words, is qualitatively different from a person merely being at the low end of the normal range.

On the genetic side, the last two decades have transformed the picture. High-resolution methods — chromosomal microarrays and, above all, whole-*exome* and whole-*genome* sequencing — have shown that a large share of moderate-to-severe intellectual disability is caused by rare, often *de novo* (newly arising, not inherited) mutations, and have pushed the diagnostic yield in unexplained cases sharply upward (Vissers, Gilissen, & Veltman, 2016). Hundreds of individual genes have now been implicated, most of them converging on a small number of biological themes — synaptic function, chromatin regulation, and the control of gene transcription — that are central to building and tuning neural circuits (Ropers, 2010). The genetics of *non-syndromic* intellectual disability, where cognitive impairment occurs without a recognisable pattern of physical features, has been especially hard-won, because there are no external clues to guide the search (Kaufman, Ayub, & Vincent, 2010).

Population data confirm how heterogeneous the causes are. In a birth-cohort study that investigated every case systematically, identifiable genetic causes accounted for a substantial and growing fraction of intellectual disability, but no single cause dominated, and a meaningful proportion remained unexplained even after thorough evaluation (Karam et al., 2015). The genetic overlap with autism spectrum disorder is also considerable: many of the same genes, when disrupted, can produce intellectual disability, autism, or both, underlining that these diagnostic categories carve up a shared underlying biology (Srivastava & Schwartz, 2014). Advancing sequencing technology continues to raise diagnostic yields and to open, for a minority of specific conditions, the prospect of targeted treatment (Ilyas, Mir, Efthymiou, & Houlden, 2020).

Worked Example

The two-group model becomes concrete when the psychometric definition is taken at face value and compared with what is actually observed. Intelligence-test scores are constructed to follow, in the population, an approximately *normal* distribution with a mean of 100 and a standard deviation of 15. The conventional intellectual-functioning threshold — two standard deviations below the mean — therefore corresponds to an IQ of 100 − (2 × 15) = 70.

How much of the population falls below that line? Converting to a standard score, an IQ of 70 is at *z* = (70 − 100) / 15 = −2.0. The proportion of a normal distribution below *z* = −2.0 is about 2.28%. If the threshold is relaxed to IQ 75 to allow for measurement error, *z* = (75 − 100) / 15 ≈ −1.67, and the proportion below rises to roughly 4.8% — so the choice of cut-off, over a plausible five-point band, more than *doubles* the population it captures.

Now compare these psychometric figures with the observed prevalence. Meta-analysis puts the actual prevalence of intellectual disability at roughly 1% — well *below* the 2.28% the IQ threshold alone would predict (Maulik et al., 2011). The gap is exactly what the two-criteria definition is for: many people who score below IQ 70 nonetheless have adequate adaptive behaviour and so are not diagnosed, which pulls the observed figure beneath the psychometric tail. Yet at the *severe* end the arithmetic runs the other way: far more people have profound intellectual disability than a smooth normal curve predicts for scores four or five standard deviations below the mean, because that tail is filled not by normal variation but by the discrete pathological causes of the second group (Reichenberg et al., 2016). A single normal distribution simultaneously *over*-predicts the mild end and *under*-predicts the severe end — which is precisely why two groups, not one, are needed to describe the whole spectrum.

Cognitive Profile

Beneath the summary IQ, intellectual disability is accompanied by a characteristic profile of limitations in the cognitive systems that support new learning — though the profile varies with cause and severity. Working memory, the capacity to hold and manipulate information over the short term, is a consistent area of difficulty: children with intellectual disability show reduced working-memory capacity across verbal and visuospatial domains, and the degree of limitation tracks the severity of the disability (Schuchardt, Gebhardt, & Maehler, 2010). Because working memory is the workspace in which comprehension, reasoning, and learning take place, a constrained workspace ramifies into almost every academic and adaptive task.

Executive functions — the control processes of inhibition, updating, and shifting that guide goal-directed behaviour — are likewise commonly impaired, and the impairment is often greater than would be expected from the general cognitive level alone (Danielsson, Henry, Ronnberg, & Nilsson, 2010). This matters for the adaptive-behaviour criterion, because the practical and social skills of everyday life depend heavily on planning, self-monitoring, and flexible control. A limitation in executive function helps explain why measured intelligence and real-world competence, though correlated, come apart: managing a life requires not only the ability to solve a problem in the abstract but the executive machinery to deploy that ability at the right moment.

Two cautions temper any single profile. First, the pattern is *heterogeneous*: different genetic causes produce different cognitive signatures, so that the uneven visuospatial-versus-verbal profile of Williams syndrome differs sharply from the profile of Down syndrome or of fragile X syndrome. Averaging across causes can therefore obscure as much as it reveals (Patel et al., 2020). Second, the profile is *developmental*: it emerges and changes over time, and the trajectory of working memory and executive control across childhood is itself part of what distinguishes intellectual disability from typical development.

Assessment and Classification

Diagnosing intellectual disability requires three things established together: significantly limited intellectual functioning, significantly limited adaptive behaviour, and onset during the developmental period. Intellectual functioning is measured with an individually administered, culturally appropriate, standardised intelligence test; adaptive behaviour with a norm-referenced measure completed by an informant who knows the person well, sampling the conceptual, social, and practical domains (Tasse et al., 2012). No single test, and certainly no IQ number alone, is sufficient; clinical judgement integrating the whole picture is explicitly built into every major framework.

A significant change in DSM-5 was to *decouple severity from the IQ score*. Where earlier systems graded intellectual disability as mild, moderate, severe, or profound chiefly by IQ band, DSM-5 grades severity by the level of *adaptive* functioning — how much support a person needs in the conceptual, social, and practical domains — on the reasoning that it is adaptive functioning, not the test score, that determines the support required (American Psychiatric Association, 2013). This aligns the classification with the AAIDD's long-standing emphasis on supports and with the ICD-11 reconceptualisation of the condition as a disorder of intellectual development (Salvador-Carulla et al., 2011). The four levels persist as useful shorthand, but they now describe *what a person needs*, not merely *how they score*.

Prevalence estimates depend heavily on these definitional choices, as well as on how cases are found. Systematic reviews report figures ranging from well under 1% to over 3% depending on the country, the age group, and whether cases are ascertained administratively or through population screening — with the adaptive-behaviour criterion and the reliance on service records both tending to lower recorded prevalence relative to the psychometric prediction (McKenzie, Milton, Smith, & Ouellette-Kuntz, 2016). The variability is not noise to be averaged away but a direct reflection of the fact that intellectual disability is defined at the intersection of ability, environment, and social response.

Development Across the Lifespan

Because intellectual disability is defined by onset in the developmental period, it is intrinsically a lifespan condition, and its expression changes with age. In early childhood it is often first suspected through delayed milestones — late talking, late walking, slow acquisition of self-care skills — and milder forms in particular may not become apparent until the academic and social demands of school exceed a child's capacities (Patel et al., 2020). This age-dependence is one reason prevalence estimates rise through childhood: the same underlying limitation becomes visible only when the environment asks more of it.

Across adolescence and adulthood the focus shifts from identification to *adaptation and support*. The adaptive-behaviour framework is explicitly forward-looking: the goal is to identify the pattern of supports that will let a person participate as fully as possible in education, work, and community life, and to adjust those supports as demands change (Schalock et al., 2010). Many people with milder intellectual disability achieve substantial independence with appropriate support; those with more severe disability need more extensive, often lifelong, assistance. Public-health and epidemiological work has increasingly documented the health inequalities that accompany intellectual disability across the lifespan, and the importance of designing services around them (McKenzie et al., 2016).

Discussion

The scientific interest of intellectual disability for cognitive psychology lies in a tension it makes unavoidable: it is defined at the level of *general* ability, yet it can only be understood by decomposing that generality into parts. The two-criteria definition — intellectual functioning *and* adaptive behaviour — is itself a claim that general intelligence and real-world competence are distinguishable, and the frequent dissociation between them, driven partly by executive function, is evidence that a single number cannot capture what it takes to run a life (Tasse et al., 2012; Danielsson et al., 2010). Intellectual disability thus does for the concept of intelligence what specific deficits do for specific faculties: it shows where the joints are.

The aetiological story reinforces the point. That a single behavioural description — below-average functioning with limited adaptive behaviour — is reached by the polygenic tail of the normal distribution *and* by hundreds of discrete genetic causes tells us that very different biological routes converge on a common cognitive outcome (Reichenberg et al., 2016; Vissers et al., 2016). For the science of mind this convergence is informative in both directions: it warns against expecting one mechanism or one profile, and it makes specific genetic causes such as Down syndrome and Williams syndrome uniquely valuable, because each is a natural experiment linking a defined biological difference to a characteristic reshaping of cognition.

Cognitive Implications

For cognitive psychology, intellectual disability is a standing reminder that intelligence is not only a psychometric quantity but a capacity that must be *enacted* in the world. The separation of intellectual functioning from adaptive behaviour, and the role of working memory and executive function in bridging the two, supports models in which general ability and the control processes that deploy it are related but distinct — and in which a limitation can lie in the deployment as much as in the underlying capacity (Danielsson et al., 2010; Schuchardt et al., 2010).

The condition also sharpens the relationship between intellectual disability and learning disabilities. The two are distinct: a learning disability is a specific difficulty (in reading, say, or arithmetic) against a background of otherwise typical general ability, whereas intellectual disability is a *general* limitation. Holding the distinction clearly is important both scientifically and practically, because it separates a circumscribed processing deficit from a broad limitation of intellectual functioning, and directs quite different kinds of support (Patel et al., 2020). And the heterogeneity of aetiology carries a practical lesson that the syndrome-comparison approach makes vivid: recognising the *specific* cognitive profile associated with a person's particular cause — rather than treating intellectual disability as uniform — is what allows teaching and support to build on genuine strengths.

Current Directions

The most active front is genetic. Whole-exome and whole-genome sequencing have turned the diagnosis of previously unexplained intellectual disability into a tractable problem, steadily raising the proportion of cases with an identified molecular cause and continuing to add genes to an already long list (Vissers et al., 2016; Ilyas et al., 2020). Beyond diagnosis, this work is beginning to deliver mechanism: as implicated genes converge on synaptic and chromatin-regulatory pathways, a minority of conditions are becoming candidates for targeted, sometimes reversible, intervention, and the prospect of gene-directed therapies — still early — is now part of the research agenda (Ilyas et al., 2020).

A second front is conceptual and public-health oriented. The reframing of intellectual disability around adaptive behaviour and needed supports, formalised in the AAIDD framework and the ICD-11 renaming, continues to shape how the condition is measured and served (Schalock et al., 2010; Salvador-Carulla et al., 2011). In parallel, epidemiological research is producing better global prevalence estimates and documenting the health inequalities that accompany intellectual disability, with the aim of designing services that reach the populations current ascertainment methods miss (McKenzie et al., 2016). Across both fronts the field increasingly treats intellectual disability not as a static deficit but as a developmental condition whose course can be understood, and supported, in fine detail.

Common Misconceptions

“Intellectual disability is just a low IQ.”

No. Diagnosis requires significant limitations in both intellectual functioning and adaptive behaviour, with onset in the developmental period. A low test score with intact everyday functioning does not qualify (Tasse et al., 2012).

“Intellectual disability is a single disorder with one cause.”

It is a final common pathway reached by hundreds of distinct causes, from the polygenic lower tail of the normal ability distribution to discrete genetic and environmental insults (Reichenberg et al., 2016; Vissers et al., 2016).

“Intellectual disability is the same as a learning disability.”

No. A learning disability is a specific difficulty against a background of otherwise typical general ability; intellectual disability is a general limitation of intellectual functioning. (Confusingly, British usage historically used “learning disability” for what this article calls intellectual disability.) (Patel et al., 2020)

“Severity is set by the IQ score.”

Not in current frameworks. DSM-5 grades severity by the level of adaptive functioning and needed support, not by the IQ band, because it is adaptive functioning that determines the support required (American Psychiatric Association, 2013).

Glossary

Adaptive behaviour.

The conceptual, social, and practical skills people learn and use in everyday life; a co-equal criterion with intellectual functioning for diagnosing intellectual disability.

Conceptual domain.

The area of adaptive behaviour covering language, literacy, money, time, and number concepts.

De novo mutation.

A genetic change arising newly in an egg, sperm, or early embryo rather than inherited from a parent; a major cause of more severe intellectual disability.

Developmental period.

The span, conventionally before adulthood, during which the limitations of intellectual disability must arise; distinguishes it from later-onset conditions such as dementia.

Executive function.

The control processes — inhibition, updating, shifting — that guide goal-directed behaviour; frequently impaired in intellectual disability.

Exome sequencing.

A method that reads all the protein-coding regions of the genome; the technique that transformed the genetic diagnosis of intellectual disability.

Intellectual functioning.

General mental capacity for reasoning, planning, problem-solving, and learning, estimated by an intelligence test and summarised as an IQ.

IQ (intelligence quotient).

A standardised score of intellectual functioning, scaled to a population mean of 100 and standard deviation of 15; the intellectual-functioning threshold is about two standard deviations below the mean.

Non-syndromic intellectual disability.

Intellectual disability occurring without a recognisable pattern of accompanying physical features, making its cause especially hard to identify.

Practical domain.

The area of adaptive behaviour covering daily living, occupational skills, health care, travel, and use of everyday tools.

Social domain.

The area of adaptive behaviour covering interpersonal skills, social responsibility, following rules, and avoiding victimisation.

Standard deviation.

A measure of the spread of a distribution; on the IQ scale it is 15 points, so an IQ of 70 is two standard deviations below the mean.

Syndromic intellectual disability.

Intellectual disability occurring as part of a recognisable syndrome with characteristic physical or medical features, as in Down or Williams syndrome.

Two-group approach.

The idea that intellectual disability comprises two overlapping populations: a milder group grading into the normal ability distribution and a more severe group with discrete pathological causes.

Working memory.

The capacity to hold and manipulate information over the short term; a consistent area of limitation whose reduction tracks the severity of intellectual disability.

Key Researchers

Alfred Binet

(1857–1911). A French psychologist at the Sorbonne who, with Theodore Simon, created the first practical intelligence scale to identify schoolchildren needing additional support — the historical root of the psychometric assessment still central to defining intellectual disability. Wikidata

Eric Emerson

(living). A British psychologist at Lancaster University whose work established the epidemiology and public health of intellectual disability, documenting its social determinants and the health inequalities that accompany it across the lifespan. ORCID

Luis Salvador-Carulla

(living). A psychiatrist at the University of Canberra who led the reconceptualisation of the condition as *disorders of intellectual development* for ICD-11, reconciling the clinical, educational, and social frameworks. ORCID

Robert L. Schalock

(living). A psychologist (Hastings College, emeritus) who was the principal architect of the modern AAIDD definition, shifting the field from a deficit-focused model toward one organised around adaptive behaviour and needed supports. ORCID

Edouard Seguin

(1812–1880). A French-American physician and educator who pioneered systematic education for people with intellectual disability, whose physiological method shaped nineteenth- and twentieth-century special education. Wikidata

Marc J. Tasse

(living). A psychologist at the Nisonger Center, Ohio State University, whose work defined and operationalised the construct of adaptive behaviour and its measurement across the conceptual, social, and practical domains. ORCID

Joris A. Veltman

(living). A human geneticist at Newcastle University who pioneered the use of exome sequencing and the study of de novo mutations in intellectual disability, transforming its genetic diagnosis. ORCID

Frequently Asked Questions

What is intellectual disability?

Intellectual disability is a neurodevelopmental condition defined by significant limitations in both intellectual functioning (reasoning, problem-solving, and learning) and adaptive behaviour (everyday conceptual, social, and practical skills), with onset during the developmental period (Tasse et al., 2012).

Is intellectual disability the same as a low IQ?

No. A low IQ is only one of the required criteria. A person must also have significant limitations in adaptive behaviour, and the limitations must have arisen during the developmental period. A low test score with intact everyday functioning is not intellectual disability (Tasse et al., 2012).

How common is intellectual disability?

Meta-analysis puts the prevalence at roughly 1% of the population, though estimates range from under 1% to over 3% depending on the definition, the age group, the country, and how cases are identified (Maulik et al., 2011; McKenzie et al., 2016).

What causes intellectual disability?

There is no single cause. Milder intellectual disability grades into the polygenic lower tail of the normal ability distribution, while more severe intellectual disability is dominated by discrete genetic causes — often de novo mutations — and by chromosomal, metabolic, infectious, and environmental factors (Reichenberg et al., 2016; Vissers et al., 2016).

How is intellectual disability diagnosed?

Through an individually administered intelligence test, a norm-referenced measure of adaptive behaviour across the conceptual, social, and practical domains, and evidence of onset during the developmental period — integrated by clinical judgement rather than decided by any single number (Tasse et al., 2012).

How are severity levels defined?

The four levels — mild, moderate, severe, and profound — were historically set by IQ band, but DSM-5 now grades severity by the level of adaptive functioning and the support a person needs, because it is adaptive functioning that determines support requirements (American Psychiatric Association, 2013).

How is intellectual disability different from a learning disability?

A learning disability is a specific difficulty (such as in reading or arithmetic) against a background of otherwise typical general ability, whereas intellectual disability is a general limitation of intellectual functioning. Note that British usage has historically used “learning disability” to mean intellectual disability (Patel et al., 2020).

Can intellectual disability be treated?

The condition itself is lifelong, and support — tailored to a person's pattern of adaptive strengths and needs — is the mainstay. For a growing minority of specific genetic causes, precise diagnosis is beginning to open the prospect of targeted intervention (Ilyas et al., 2020).

Support Organizations

• American Association on Intellectual and Developmental Disabilities (AAIDD) — the professional organisation that maintains the leading definition and classification framework for intellectual disability.
• The Arc — a major US organisation advocating for and serving people with intellectual and developmental disabilities and their families.
• Mencap — the leading UK charity for people with a learning disability (the British term for intellectual disability), providing support, information, and advocacy.
• MedlinePlus: Developmental Disabilities — an accessible, authoritative overview from the US National Library of Medicine.

References

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). American Psychiatric Publishing. https://doi.org/10.1176/appi.books.9780890425596

Danielsson, H., Henry, L., Ronnberg, J., & Nilsson, L. G. (2010). Executive functions in individuals with intellectual disability. Research in Developmental Disabilities, 31(6), 1299–1304. https://doi.org/10.1016/j.ridd.2010.07.012

Ilyas, M., Mir, A., Efthymiou, S., & Houlden, H. (2020). The genetics of intellectual disability: Advancing technology and gene editing. F1000Research, 9, 22. https://doi.org/10.12688/f1000research.16315.1

Karam, S. M., Riegel, M., Segal, S. L., Felix, T. M., Barros, A. J. D., Santos, I. S., Matijasevich, A., Giugliani, R., & Black, M. (2015). Genetic causes of intellectual disability in a birth cohort: A population-based study. American Journal of Medical Genetics Part A, 167(6), 1204–1214. https://doi.org/10.1002/ajmg.a.37011

Kaufman, L., Ayub, M., & Vincent, J. B. (2010). The genetic basis of non-syndromic intellectual disability: A review. Journal of Neurodevelopmental Disorders, 2(4), 182–209. https://doi.org/10.1007/s11689-010-9055-2

Maulik, P. K., Mascarenhas, M. N., Mathers, C. D., Dua, T., & Saxena, S. (2011). Prevalence of intellectual disability: A meta-analysis of population-based studies. Research in Developmental Disabilities, 32(2), 419–436. https://doi.org/10.1016/j.ridd.2010.12.018

McKenzie, K., Milton, M., Smith, G., & Ouellette-Kuntz, H. (2016). Systematic review of the prevalence and incidence of intellectual disabilities: Current trends and issues. Current Developmental Disorders Reports, 3(2), 104–115. https://doi.org/10.1007/s40474-016-0085-7

Patel, D. R., Cabral, M. D., Ho, A., & Merrick, J. (2020). A clinical primer on intellectual disability. Translational Pediatrics, 9(Suppl. 1), S23–S35. https://doi.org/10.21037/tp.2020.02.02

Reichenberg, A., Cederlof, M., McMillan, A., Trzaskowski, M., Kapra, O., Fruchter, E., Ginat, K., Davidson, M., Weiser, M., Larsson, H., Plomin, R., & Lichtenstein, P. (2016). Discontinuity in the genetic and environmental causes of the intellectual disability spectrum. Proceedings of the National Academy of Sciences, 113(4), 1098–1103. https://doi.org/10.1073/pnas.1508093112

Ropers, H. H. (2010). Genetics of early onset cognitive impairment. Annual Review of Genomics and Human Genetics, 11, 161–187. https://doi.org/10.1146/annurev-genom-082509-141640

Salvador-Carulla, L., Reed, G. M., Vaez-Azizi, L. M., Cooper, S. A., Martinez-Leal, R., Bertelli, M., Adnams, C., Cooray, S., Deb, S., Akoury-Dirani, L., Girimaji, S. C., Katz, G., Kwok, H., Luckasson, R., Simeonsson, R., Walsh, C., Munir, K., & Saxena, S. (2011). Intellectual developmental disorders: Towards a new name, definition and framework for “[intellectual disability]” in ICD-11. World Psychiatry, 10(3), 175–180. https://doi.org/10.1002/j.2051-5545.2011.tb00045.x

Schalock, R. L., Borthwick-Duffy, S. A., Bradley, V. J., Buntinx, W. H. E., Coulter, D. L., Craig, E. M., Gomez, S. C., Lachapelle, Y., Luckasson, R., Reeve, A., Shogren, K. A., Snell, M. E., Spreat, S., Tasse, M. J., Thompson, J. R., Verdugo-Alonso, M. A., Wehmeyer, M. L., & Yeager, M. H. (2010). Intellectual disability: Definition, classification, and systems of supports (11th ed.). American Association on Intellectual and Developmental Disabilities.

Schuchardt, K., Gebhardt, M., & Maehler, C. (2010). Working memory functions in children with different degrees of intellectual disability. Journal of Intellectual Disability Research, 54(4), 346–353. https://doi.org/10.1111/j.1365-2788.2010.01265.x

Srivastava, A. K., & Schwartz, C. E. (2014). Intellectual disability and autism spectrum disorders: Causal genes and molecular mechanisms. Neuroscience & Biobehavioral Reviews, 46, 161–174. https://doi.org/10.1016/j.neubiorev.2014.02.015

Tasse, M. J., Schalock, R. L., Balboni, G., Bersani, H., Borthwick-Duffy, S. A., Spreat, S., Thissen, D., Widaman, K. F., & Zhang, D. (2012). The construct of adaptive behavior: Its conceptualization, measurement, and use in the field of intellectual disability. American Journal on Intellectual and Developmental Disabilities, 117(4), 291–303. https://doi.org/10.1352/1944-7558-117.4.291

Vissers, L. E. L. M., Gilissen, C., & Veltman, J. A. (2016). Genetic studies in intellectual disability and related disorders. Nature Reviews Genetics, 17(1), 9–18. https://doi.org/10.1038/nrg3999