Genetic basis of poor scholastic performance among

children: A review

Kavita Singh, Dinesh Parmar and CBS Dangi

Department of Biotechnology, RKDF University, Bhopal (Madhya Pradesh) India

ABSTRACT

This paper presents concise reviewon selective pioneering works and recent progress on the topic genetic basis of

poor scholastic performance among children. Formal school education plays a great role in everyone’s life. Poor

scholastic performance may be the result of Intellectual disability or mental retardation which manifests under age

18. Interaction of certain genes and environmental conditions can result in intellectual disabilities. This provides

ample de nitions of concepts, classi cation, causes and consequences, prevalence, and involvement of chromosomes

in mental disability cases. This reveals that the magnitude of genetic variations in mental de ciency and scholastic

performance of children suggests strong genetic component.

KEY WORDS: SCHOLASTIC PERFORMANCE SCHOOL CHILDREN GENETIC REASONS

766

Genetical

Communication

Biosci. Biotech. Res. Comm. 11(4): 766-772 (2018)

INTRODUCTION

Formal school education plays a great role in every-

one’s life. Unsettled poor scholastic performance poses

instant and lifelong unfavorable effects on a child and

adolescent’s growth and cognitive development. Opti-

mum cognitive development of a child in uences his/

her learning behavior which is in uenced by interac-

tion of family, society, psychology, education, and eco-

nomical atmosphere of the child. Poor scholastic perfor-

mance is observed among some children (Carlson and

Corcoran, 2001; Landry, 2014). Interactions of Gene and

environment can result in different disease phenotypes

and intellectual abilities (McKusick, 1983; Deary, 2012).

All traits of an individual are products of heredity and

environ ment interaction. Individuals with varied gen-

otypes appear differently by exposure to the common

environmental factors (Davies, 2016). Intelligence was

one of the  rst human traits to be the target of genetic

research even before psychology emerged as a scien-

ARTICLE INFORMATION:

Received 6

Oct, 2018

Accepted after revision 25

Dec, 2018

BBRC Print ISSN: 0974-6455

Online ISSN: 2321-4007 CODEN: USA BBRCBA

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BIOSCIENCE BIOTECHNOLOGY RESEARCH COMMUNICATIONS GENETIC BASIS OF POOR SCHOLASTIC PERFORMANCE AMONG CHILDREN: A REVIEW 767

Kavita Singh, Dinesh Parmar and CBS Dangi

ti c  eld. The correlation between DNA sequence and

behavioral differences such as intelligence is considered

causal because DNA variations can lead to behavioral

differences but behavioral differences do not change

DNA sequences (Deary et al., 2006; Sniekers et al., 2017).

Intellectual disability and Poor Scholastic Performance

The“poor scholastic performance” is a broad term and

de ned differently by scholars. Okoye (1982) de ned

poor scholastic performance as one in which a student

is not successful in attaining standard performance in a

speci ed evaluation exercises involving a test, an exam-

ination or a set of constant assessment. Poor scholastic

performance may be the result of Intellectual disabil-

ity or mental retardation which manifests under age 18.

American Association on Mental Retardation (AAMR)

and American Psychiatric Association (APA) de ne

mental retardation on the basis of certain formulations

developed by them. This refers to extensive limitations

in functioning characterized by radically sub-average

intellectual level, existing concurrently with limitations

in two or more of the following adaptive skill areas:

communication ability, self-care, social skills, self-direc-

tion, community use, health and safety, leisure, home

living and work (Luckasson et al. 1992).

The AmericanPsychiatricAssociation (APA) is respon-

sible for naming, de ning, and describing mental dis-

orders. Fifth edition of the Diagnostic and Statistical

Manual ofMentalDisorders (DSM-5), APA changed the

term mental retardation and proposed the new term intel-

lectual disability or intellectual developmental disorder.

De nition of Concepts

De ning mental retardation remains a challenge and a

matter of controversy. Ever since people have been able

to distinguish mental retardation from other forms of

mental disability, a central theme of de nitions has con-

cerned the failure of mentally retarded persons to adapt

adequately to their surroundings. Older de nitions were

couched in terms of adult behavior, and there was a ten-

dency to avoid precise criteria for deciding in borderline

instances.

Many writers have attempted to specify quantita-

tive standards for deciding mental subnormal level. The

most widely used objective criterion of this sort has

been the score obtained on a standardized test of intel-

ligence such as the Stanford-Binet Intelligence Scale or

the Wechsler Intelligence Scale for Children (WISC). In

1916, Terman introduced a grouping of ability accord-

ing to IQ’s obtained on the Stanford-Binet (Terman and

Merrill, 1937). This system became widely used and, in

fact, became the standard classi cation system (Table

1). An IQ of 70 has gained considerable popularity as a

cutoff score for the retarded group.

Doll (1953) provided more speci c de nition. In addi-

tion to the element of social adaptation, he emphasized

the emergence of handicap in childhood, its constitu-

tional nature and its incurability. He considered some

criteria generally considered essential to an adequate

de nition and concept. These involve social incompe-

tence, mental sub-normality, developmentally arrested,

obtained at maturity, constitutional origin and essen-

tially incurable. Tredgold (1956) de ned mental de -

ciency as a state of incomplete mental development of

such a kind and degree that the individual was incapable

of adapting himself to the normal environment of his

fellows in such a way as to maintain existence indepen-

dently of supervision, control or external support.

The American Association on Mental De ciency

de nes mental retardation as a signi cantly sub-aver-

age general intellectual function existing concurrently

with de cits in adaptive behavior, and manifested dur-

ing the developmental period. In this de nition the

retarded person is judged in terms of his success with

the developmental tasks appropriate for his age: in the

preschool period sensorimotor behaviors assume great-

est importance, while during the school years academic

ability is of  rst interest, and during adulthood eco-

nomic independence and social recognition (Suess et al.,

1983; APA, 2000). Furthermore, this de nition makes

it clear that a designation of mental status should be a

description of present behavior and implicitly disowns

the notion of potential intelligence.

There are a number of dif culties with these scoring

criteria. Because an IQ is simply a score obtained on the

basis of a restricted sample of behavior, there are signi -

cant limitations as to what can or should be expected of

it, even if the tests are perfectly reliable and children are

always able to put forth their best efforts. Furthermore, no

cutoff score will ever be adequate to de ne mental retar-

dation independent of the setting in which the individual

 nds himself. Different skills and abilities are required at

different ages and in different environments. Retardation

must therefore be gauged in large part against current

environmental demands, (Reschly et al., 2002).

Apart from this, the cutoff scores for measures of

intellectual function are better recognized than the cutoff

scores for measures of adaptive behavior. There is open

agreement in the major diagnostic systems that perfor-

mance on the intellectual dimension must be approxi-

mately two or more standard deviations below the popu-

lation mean, which translates into an IQ score of 70 or less

on measures with a mean of 100 and a standard deviation

of 15 (Reschly et al. 2002; Greene et al., 2004).

Classi cation systems

Mentally Retarded or intellectually disabled individu-

als comprise a very heterogeneous group both in their

768 GENETIC BASIS OF POOR SCHOLASTIC PERFORMANCE AMONG CHILDREN: A REVIEW BIOSCIENCE BIOTECHNOLOGY RESEARCH COMMUNICATIONS

Kavita Singh, Dinesh Parmar and CBS Dangi

behavior and in the causes of their de ciency. Different

classi cation systems have been proposed in the past

to bring some order in this disarray. Most systems have

approached the problem from one of three viewpoints:

severity of the handicap, etiology of the symptoms, and

the symptom collection.

Additional criteria for classi cation

Persons with mental retardation can also be grouped by

age, an important criterion in education and longitudinal

evaluation. Mainly for purposes of management, mental

retardation can also be subdivided according to the bio-

logical syndrome. This classi cation offers advantages

for special training and schooling in mentally retarded

patients with associated de cits such as blindness, deaf-

ness, and spina bi da, (Halgin and Whiteborne, 2005).

Causes and Consequences

The causes of poor scholastic performance can be

broadly classi ed into two groups that involve genet-

ics and environment. The present study exclusively aims

to focus on genetic causes of PSP however, discussion

on medical and varied environmental factors remains

imperative. There may be genetic basis of various medi-

cal problems associated with PSP, and many problems

are purely environmental in their origin. Poor scholas-

tic performance (PSP) shows multiple etiologies. Many

reasons are responsible for poor scholastic performance

of children involving speci c learning disability, atten-

tion de cit hyperactivity disorder, low IQ level, emo-

tional problems and psychiatric disorders. Other reasons

involve a poor socio-cultural home environment and

additional environmental causes, (Bruno and Njoku,

2012).

The causes of PSP can be further divided into extrin-

sic or environmental and intrinsic or individual factors.

School dif culty (SD) and learning disability (LD) are

two different manifestations of some school attending

children. Former is related to pedagogical dif culties.

Apart from diseases and related disabilities, pedagogical

dif culties can also pose poor scholastic performance.

It is extrinsic in nature with no possibilities of organic

impairment (Siqueira and Gurge-Giannetti, 2011). Envi-

ronmental reasons may infuse lack of interest in stud-

ies and distraction among some children may results in

disappointment, frustration, low self-esteem and failure

(Karande and Kulkarni, 2005).

Emotional causes are also important while consid-

ering poor scholastic performance being secondary to

environmental factors involving lack of inspiration, low

self-esteem and lack of sympathy and unresponsive-

ness (Valiente et al. 2012). It is argued that emotions

in uence school performance of children and that inte-

grating cognition and emotion can demonstrate school

performance and scholastic achievement in early for-

mal education (Blair, 2002; Raver, 2002). Therefore, for

a  ourishing learning process, numerous cognitive skills

associated with proper opportunities are essential.

Present work exclusively focuses on genetic causes of

Poor scholastic performance hence; this largely involves

Mental De ciency (MD) which is again a developmen-

tal disability characterized by sub-mental level or lower

than average intelligence of the age of a child. This is

chie y associated with biological causes that may show

developmental delay or/and involvement of genes or

chromosome. The investigation of the genetic basis of

mental de ciency focuses mainly on identi cation of

smaller and smaller chromosome variations associated

with disease, (Raynham et al., 1996; Lucy Raymond and

Tarpey, 2006).

The modest beginning of the investigation of the

genetic basis of mental de ciency started long back in

1938 with a preliminary study of patients con ned to

hospital institutions (Penrose, 1938). In later years focus

was on identi cation of smaller and smaller chromo-

some variations associated with disease (Raynham et al.,

1996; Raymond and Tarpey, 2006 ).

Abnormal development of a child that leads to men-

tal retardation may be due to trauma before birth caused

by an infection or exposure to alcohol, drugs, or other

toxins and trauma during birth caused by deprivation

of oxygen or premature delivery of a new born child.

Inherited disorders involve point mutation(s) and gross

chromosomal abnormalities. Certain point mutations

cause metabolic disorders that lead to mental retarda-

tion phenotype such as phenylketonuria (PKU). On the

Table 1. showing WHO List of Causal Factors of

Mental Retardation

S. No. Causal factors

Infections and intoxications

Trauma and physical agents

Disorders of metabolism, growth or nutrition

Gross brain damage (postnatal)

Diseases or conditions due to unknown prenatal

in uences

Chromosome abnormalities

Prematurity

Major psychiatric disorder

Psycho-social (environmental) deprivation

10.

Other and unspeci ed

Source: WHO: Mental health: strengthening our response (www.

who.int/news-room/fact-sheets/detail/mental-health-strengthening-

our-response)

BIOSCIENCE BIOTECHNOLOGY RESEARCH COMMUNICATIONS GENETIC BASIS OF POOR SCHOLASTIC PERFORMANCE AMONG CHILDREN: A REVIEW 769

Kavita Singh, Dinesh Parmar and CBS Dangi

other hand, chromosomal abnormality such as Down

syndrome demonstrates peculiar morphological and

abnormal behavioral traits. The averageIQof matured

persons with Down syndrome remains 50 that remain

widely variable, (Malt et al. 2013).

Prevalence

Social integration of a moderately mental retardate will

be more dif cult in a competitive, industrialized com-

munity than in a rural environment with the long-term

support of an old fashioned, extended family (Durkin et

al. 1995). Almost all studies dealing with mental sub-

normality in children report a higher incidence in males

than in females. Moreover, in addition to the data col-

lected from population and institution surveys, recent

studies of family pedigrees more speci cally demonstrate

that X-linked recessive disorders represent a substantial

proportion of mentally retarded males (Raymond, 2006).

The prevalence of mental retardation is in uenced by

a great number of environmental factors such as com-

munity, age, racial and ethnic background, geographic

region, and sex (Hernandez and Blazer, 2006).

According to WHO estimates globally more than 450

million people suffer from mental disorders. Currently,

mental and behavioral disorders account for 12% of the

global burden of disease. This is likely to increase to

15% by 2020. The major proportions of mental disor-

ders come from low- and middle-income countries. The

problem is further complicated by a lack of adequate

trained manpower and a low priority of mental health in

health policy (Reddy et al. 2013).The severely retarded

are mostly identi ed before the age of one year, espe-

cially in the presence of physical abnormalities such

as hydrocephaly, spasticity, and sensorial disturbances.

Mildly mentally retarded individuals with IQ’s ranging

between 50 and 70 are recognized at school age (Boat

and Wu, 2015).

In India, mental disorders have a prevalence of

1.05%. Urban population has slightly higher rate being

at 1.1% as compared to rural being at 1.008%. Age was

found to be highly correlated with prevalence among

children of rural areas (Lakhan et al. 2015). Once the

critical period of adolescence and school attendance

is over, however, many of the mildly mentally handi-

capped are assimilated into society and join the ranks

of the dull-normal, living for the most part in marginal

socio economic circumstances.

Genetic Disorders

Genetic disorders are divided into two main groups.

The  rst group includes chromosome disorders, such as

Down syndrome, which may involve an entire chromo-

some including thousands of genes, while the second

group involves only a single gene. Single gene disorders

are divided into three main categories based on the mode

of inheritance of the abnormal gene. The categories are

autosomal recessive, autosomal dominant, and X-linked

(Thompson and Thompson, 1986; Pradhan et al., 2011).

Involvement of Chromosomes in Mental Disability

There are genetic components to mental disability.

Examination of persons with chromosomal variations

and mental disabilities may be a way of overcoming

dif culties faced with the proper diagnostic processes.

Unfortunately, chromosomal analysis is rarely under-

taken in subjects with psychiatric disorders. However,

the rate of chromosomal abnormality has signi cantly

increased in persons with learning disability, and may

be as high as 20% in those with mild learning dis-

ability (Gostason et al. 1991).It has been established

in many other medical conditions with a genetic basis

that chromosomal variations, either by direct gene dis-

order or by positional effects, can produce identical or

similar phenotypes to those caused by point mutations

and their existence has greatly facilitated the physi-

cal mapping and cloning of candidate genes (Collins,

1992, 1995).

Once a chromosomal anomaly is detected in a sub-

ject with mental disability, it may be considered non-

coincidental and related to the disorder if one or more

of the following criteria are met: (a) the chromosomal

abnormality is rare and there are independent reports of

the abnormality being associated with mental disability;

(b) there is proximity of the abnormality with a region

of suggestive linkage  ndings; or (c) there is co-segre-

gation of the abnormality with mental disability within

the patient’s family, (Evans et al. 2001).

Some variations in chromosomes are very small and

they only involve a single gene called single gene dis-

orders. However, when variations in chromosomes are

large enough and can be seen under light microscope,

they are called chromosome anomalies or aberrations.

There are many types of chromosome anomalies. Chro-

mosome anomalies usually occur when there is an error

incell divisionfollowingmeiosisormitosis. They can be

organized into two basic groups viz. Numerical anom-

alies (aneuploidy or an abnormal number of chromo-

somes) and Structural anomalies. Numerical anomalies

occur due to nondisjunction where abnormal numbers

of chromosomes may  nd their way into gametes, and

a disorder of chromosome numbers may result. Altera-

tion in chromosome structure can take several forms

described as under:

• Deletions: A portion of the chromosome is missing

or deleted.

• Duplications: A portion of the chromosome is

duplicated

770 GENETIC BASIS OF POOR SCHOLASTIC PERFORMANCE AMONG CHILDREN: A REVIEW BIOSCIENCE BIOTECHNOLOGY RESEARCH COMMUNICATIONS

Kavita Singh, Dinesh Parmar and CBS Dangi

• Translocations: A portion of one chromosome is

transferred to another chromosome. There are two

main types of translocations:

Reciprocal translocation: Segments from two dif-

ferent chromosomes have been exchanged.

Robertsonian translocation: An entire chromo-

some has attached to another at the centromere

• Inversions: A portion of the chromosome has

broken off, turned upside down, and reattached,

therefore the genetic material is inverted.

There are two main types of Inversions:

Paracentric inversions: Both breaks occur in

one arm of the chromosome and do not include

thecentromere

Pericentric inversions: Breaks occur in each arm

of the chromosome and involved the centromere

• Insertions: A portion of one chromosome has been

deleted from its normal place and inserted into

another chromosome.

• Rings: A portion of a chromosome has broken off

and formed a circle or ring. This can happen with

or without loss of genetic material.

• Isochromosome: Formed by the mirror image copy

of a chromosome segment including the cen-

tromere.

The chromosomes observed at metaphase stage pos-

sess two chromatids called sister chromatids. Chroma-

tids of two different chromosomes are called non-sister

chromatids. Conventionally, all the chromosomal aber-

rations are broadly divided into two groups.

Chromosome-type: In this type, breaks and re-joins

always involvebothsister-chromatids at any one locus.

Chromatid-type: In this type, breaks and re-joins

always involveonlyoneof the sister-chromatids at any

one locus.

Common Chromosomal Anomalies in Mental De ciency

Down syndrome

Down syndrome is unique in its prominent role in

exploring biology of mental retardation for the  rst

time in 1866 by John Longdon Down whose contribu-

tion was signi cant in understanding biology of normal

and abnormal development (Down, 1866). The discovery

of an extra 21 chromosome (trisomy 21) in the cells of

individuals with Down syndrome exhibiting 47 chro-

mosomes in place of 46 normal numbers by Professor

Lejeune in 1959 established role of chromosome varia-

tions in development.

This was the discovery of chromosome aneuploidy in

man that  rmly established study of chromosome called

cytogenetic as bona  de medical discipline (Smith and

Warren, 1985; Patterson, 2009). Karyotype of normal

human exhibits that chromosome 21 is one of the small-

est autosomes, comprising nearly 1.9% of human DNA,

Non-disjunction of this autosome during formation of

the gametes at meiosis I or meiosis II in one of the par-

ents result in Down syndrome. Down syndrome is the

most common genetic form of mental retardation fol-

lowed by X-linkedmental retardation.

Fragile X syndrome

Fragile sites are heritable points on a chromosome which

are susceptible to breakage and are consistently found on

certain human chromosomes (Sutherland, 1982a, 1982b).

These sites may represent structural chromosome muta-

tions. Fragile X syndrome (FXS) causes learning disabil-

ities and cognitive impairment. Usually, the penetrance

of this genetic condition is higher in males as compared

to females because males are hemizygous having sin-

gle X-chromosome (McKusick, 1983). The maximum

numbers of single genes that cause mental retardation

are located on X chromosome. The  rst identi ed gene

was FMR1 that causes fragile X syndrome being the

commonest single gene abnormality. The fragile site on

the long arm of the X (Xq 27.3) is associated with a form

of familial X-linked mental retardation (Lubs, 1969). It

has been estimated that from one third to one half of all

families with (nonspeci c) X-linked mental retardation

express the fragile site in some proportion of their cells

(Brookwell et al, 1982).

The fragile site can be detected in chromosome prepa-

rations from lymphocytes grown in tissue culture media

lacking folic acid and thymidine. Speci c culture condi-

tions can signi cantly alter the frequency with which

the fragile site is expressed. Female carriers of this disor-

der may or may not express the fragile Xj some express

it in only a small number of their cells. Thus, Xq fragile

site demonstration in such carriers and in some affected

males may be dif cult due to a low level of expression.

As with most X-linked recessive disorders, carrier detec-

tion is an important: aspect of genetic counseling for

families with this syndrome.

Males with fragile X syndrome show mild to moder-

ate intellectual disability whereas considerable propor-

tions of females with this disorder being nearly one-third

remain intellectually disabled. Majority of males and

nearly half the females withfragile X syndromeshow

characteristic morphological features involving long

and narrowface, prominent jaw and forehead,  atfeet,

large ears and in males additionally enlarged testicles

after puberty. A mutation of FMR-1 known as fragile-X

mental retardation gene located on the X- chromosome

causes this syndromic condition. The FMR1 gene codes

a protein known as fragile X mental retardation protein

(FMRP) required for normal brain development. Inci-

dence was noted in all races and ethnic groups. Nearly

BIOSCIENCE BIOTECHNOLOGY RESEARCH COMMUNICATIONS GENETIC BASIS OF POOR SCHOLASTIC PERFORMANCE AMONG CHILDREN: A REVIEW 771

Kavita Singh, Dinesh Parmar and CBS Dangi

10% affected males have severe intellectual disability

(Hagerman and Hagerman, 2002).

In fragile X syndrome, CGG pattern in a part of DNA

in FMR1 gene is repeated many times. In majority of

persons, the number of repeats remains small at 5 to 44

repeats, which is common whereas; when the number of

repeats is very high being greater than 200 repeats, the

gene turns off and protein production is halted leading

to development of FXS which is also known as trinucle-

otide repeat disorder. This is heritable condition trans-

mitted from parents. Intermediate number of repeats at

nearly 45 to 54 may have somewhat higher probability

of having some symptoms but they do not have fragile

X syndrome (Willemsen et al. 2011).

Sequence repeats in the range of 55-200 do not

develop FXS but there may be development of other

condition known as fragile X-associated disorder. Cou-

ple with premutation can transmit this to their children

with the same condition or full mutation leading to

development of FXS (Gallagher andHallahan, 2012).

The global prevalence of fragile X syndrome (FXS) in

males is estimated nearly 1 in 4,000 while in females it

is nearly 1 in 5,000. It has been demonstrated in both

animal and human studies that changes in the environ-

ment radically impact behavior, (Restivo et al. 2005).

A peaceful high quality home environment has been

found associated with fewer autistic behaviors, higher

IQ scores and better adaptability in children with Fragile

X syndrome (Glaser et al. 2003).

The magnitude of genetic variations in mental de -

ciency and scholastic performance of children suggests

strong genetic component. Genetic effects that in uence

general and verbal cognitive ability are largely respon-

sible for scholastic performance. Remedial intervention

remains a more immediately attainable goal while Sub-

sequent research will entail more genetic analyses lead-

ing to identi cation of genes that in uence academic

achievement.

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