Neurolinguistics and language psychology are responsible for studying dyslexia.

The applied science that studies its treatment is psychopedagogy.

The professionals who study it are normally graduates specialized in brain and learning, such as neuropsychologists and learning psychologists/psychopedagogues (psychopedagogy).

The treatment of dyslexia must be carried out by specialized professionals, such as neuropsychologists and psychopedagogues, speech therapists (speech therapy) or teachers specialized in learning disorders.

Age at diagnosis and duration of disorder

The signs of dyslexia may vary as the child grows.[9]​.

In general, these disorders are observed for the first time when the subject is learning to read, although they may be latent long before.[10]​ At the same time, it may happen that dyslexia is not diagnosed until many years later. For example, it is common for children who have a high IQ to compensate for this pathology and it goes unnoticed until the comprehension demands increase at school.

There is debate about whether the disorder lasts a lifetime and only its consequences are minimized or whether it disappears thanks to treatments. However, there is agreement that the sooner rehabilitation work begins, the fewer the consequences will be.

Evolutionary course

From 3 to 5 years old, dyslexic children may have slow speech development and pronunciation difficulties, although there do not always have to be difficulties related to oral language.

Some authors also claim that difficulties may appear in learning routines and memorizing numbers, letters, days of the week, songs or colors; difficulties with handling their clothing (buttoning or zipping), etc. However, there is controversy about whether this is more typical of dyslexia or other learning disorders, such as, for example, teachers specializing in therapeutic pedagogy or hearing and language.

In this period it is important to observe how the literacy learning requirements are met. Despite this, it is rare to diagnose dyslexia subjects before the beginning of school, as they have only faced reading tasks.

Between 6 and 8 years old, the biggest complication they present is in the grapheme-phoneme (letter-sound) association.

Other difficulties that appear more rarely in the literature are difficulties in spatial logic operations and in sequential memory.

In some cases, deficits begin to appear in other academic areas, such as mathematics (dyscalculia). In most cases, this dyscalculia is not primary, but is due to difficulties in understanding the problem statements.

In this same age range and up to approximately 11 years old, the child can confuse numbers, letters or change their order in words; He has difficulties in pronouncing the words he reads and has difficulty understanding the readings.

Later and until adulthood, the most important difficulties appear in the comprehension of texts and are greater the more complex the text read.

Cognitive explanation of the symptomatological evolution

From the psychological paradigm of information processing, these difficulties are explained because people without dyslexia automate processes that people with the disorder have difficulty automating.

For these theories, the brain has limited processing capabilities and, if these are exceeded, processes slow down or even errors are made. That is why young children read slowly, make errors in grapheme-phoneme (letter-sound) decoding and have great difficulties in understanding. Furthermore, they have more difficulties with less known or longer words because they require more cognitive resources.

Subsequently, as children automate the reading mechanics, they have more and more resources to dedicate to understanding the text; and finally even this is largely automated.

In subjects with dyslexia, this automation occurs to a lesser extent, so they make errors for much longer, and even as adults, when at first glance the speed and precision of the reading mechanics seem correct, they have comprehension difficulties as they continue to use most of their resources in grapheme-phoneme decoding. Likewise, it is common for adults with dyslexia to continue making more errors and to be slower than the control groups in reading invented or unusual words.

Specific characteristics of dyslexia

There are certain characteristics that always occur and that need to be observed spatially:[11]​.

• - Difficulties in written language.

• - Difficulties in writing.

• - Serious difficulties with spelling.

• - Slow learning to read.

• - Difficulties in learning and writing second languages.

On the other hand, often the following may occur:

• - Difficulties in mathematics.

• - Difficulty following instructions and complex sequences of tasks.

• - Problems understanding written texts.

• - Very significant fluctuations in capacity.

Sometimes they can occur depending on the type of dyslexia or how it has affected the person:

• - Difficulties in spoken language.

• - Problems with the perception of distances and space.

• - Confusion between right and left.

• - Problems with rhythm and musical languages.

Contenido

Tiempo atrás, el tratamiento de la dislexia se anclaba en la idea del refuerzo del área de lateralidad, la orientación espacial, la grafomotricidad, la orientación temporal y las seriaciones. Sin embargo, este tipo de tratamientos están prácticamente abandonados hoy en día.[12]​.

Existe en la actualidad gran cantidad de material específico para prevenir la dislexia, entendido este como un recopilatorio de ideas para mejorar su práctica docente. Entre ellas cabe destacar el uso de los materiales elaborados por el profesor, contribuyendo de esta manera a la enseñanza más individualizada que necesitan los alumnos con rasgos disléxicos.[13]​[13]​[14]​[15]​ Dicho material específico suele estructurarse en orden de dificultad y también por edades.[16]​.

General instructions

A maxim that should guide treatment is "overlearning." That is, relearning reading and writing, but adapting the pace to the child's possibilities.

We must also take into account that both at school and at home, for a dyslexic child, schoolwork will take up more time and effort than for any other child, which sometimes turns it into arduous and tiresome work and, therefore, a task that causes frustration and rejection.

Therefore, in re-education it is important to find activities that are motivating for the child, bringing them closer to reading and writing in a more playful way.

Furthermore, the treatment will depend on the age and developmental stage of the child. The need for this differentiated treatment is closely linked to the changes in the course of the disorder.

According to age

In childhood it will be essential to influence reading requirements in a preventive manner and, consequently, on all children. Among all of them, increasing phonological awareness will be key. For this, oral materials will be used (reading has not yet begun), in which children will have to create rhymes, derive words, divide words into syllables, etc.

Between ages 7 and 10, the objectives will be, on the one hand, to increase phonological awareness, both oral and written; and on the other hand, improve the automation of reading mechanics. For the first, resources similar to those of the previous stage will be used; For the second, we will try to get the child to practice reading aloud as much as possible.

Both at this time and in subsequent times, it is essential that the subject read as much as possible as a way to improve their skills. However, this is not an easy task, since reading can be an exhausting and unpleasant task for a child or adult with dyslexia.

Therefore, it will be essential to find texts appropriate to the age and interests of the subject and motivate them so that reading is an attractive activity. Along these lines, it will also be essential to make parents and teachers of these ages aware of the child's difficulties, so that they are not pushed beyond their capabilities or feel inferior to their peers.

From the age of 10 it has been proven that it is difficult to increase phonological awareness and automation of reading. From this moment, the objectives will be different, fundamentally seeking to teach text comprehension strategies (keyword search, underlining, summary, etc.).

Compensation strategies

It will be in the last stage (from the age of 10) when it will be interesting to propose compensation strategies for the deficits, as a complement to rehabilitation. Compensation strategies are all those that, without modifying the subject's deficient abilities, facilitate their adaptation to daily life by relying on their strengths.

Some helpful instruments may be calculators, voice recordings, data tables or the presence of an adult helping with the oral reading of the study material.

Word processors are also interesting by instantly correcting many of the spelling mistakes and assisting in writing with the support of personalized and themed dictionaries that suggest words.

Controversial therapies

There are many therapies that ensure quick or almost miraculous cures; that enjoy great diffusion in the world; and yet they do not have studies that sufficiently support their usefulness or that they are even discouraged.

The following therapies are at best currently not sufficiently supported by scientific studies; In other cases they start from assumptions that do not agree with the current knowledge of dyslexia.

Before deciding on a treatment, it seems essential to find out from reliable sources whether its effectiveness has really been proven.

Text modified from Journal of Neurology; 2000; 31 (4).

1. • Optometric visual training (optometry): it is based on the theory that dyslexia is due to a visual defect and consists of visual tracking exercises, binocular control, etc. A clear and defined position regarding the non-use of visual training beyond the management of basic visual dysfunction was expressed in a joint statement issued by the Committee on Children with Disabilities, of the American Academy of Pediatrics and an ad hoc working group of the American Association of Pediatric Ophthalmology and Strabismus and the American Academy of Ophthalmology.

2. • Colored lenses: it is based on Irlen's theories and although this method has enjoyed great publicity since the 1980s as a treatment for dyslexia, there are not enough scientific studies to prove its effectiveness.[17]​[18]​.

3. • Cerebellar-vestibular training: it is based on theories that affirm that the underlying problem of dyslexia is actually a problem of the cerebellum and the ear (balance centers); and consists mainly of exercises aimed at improving stability, or antivertigo drugs. There is no evidence to support either this theory or the treatments it proposes.

4. • Sensory integration therapy: is based on the theory that learning problems and motor problems are due to a sensory integration deficit. Its ineffectiveness has been proven compared to other intervention programs.

5. • Electroencephalographic feedback (EEG Biofeedback): it is based on the assumption that both in dyslexia and in other disorders (for example, attention deficit/hyperactivity) there is an abnormal underlying brain functioning. Thus, the defenders of this therapy consider that if the electroencephalographic patterns are modified, the external difficulties will also be modified. In addition to its high cost, the studies that have reported its usefulness so far are inadequate from a methodological point of view. The groups were small and without appropriate controls.

La dislexia es un trastorno altamente poligénico con una arquitectura genética compleja. Estudios familiares han estimado que este trastorno presenta una heredabilidad del 70%.[19]​ Por lo tanto, actualmente, las investigaciones en el campo de la dislexia buscan identificar los factores de riesgo genético asociados con esta condición. Estos esfuerzos no solo contribuirán a mejorar la comprensión de los mecanismos biológicos que subyacen a esta enfermedad, sino que también podrían mejorar las técnicas de diagnóstico, permitiendo la identificación temprana de personas susceptibles a la dislexia.[20]​.

GWAS studies

With the aim of studying these genetic risk factors associated with dyslexia, numerous genome-wide association studies (GWAS) have been carried out on the genome of patients to better understand the genetic component of this disease and design new biomarkers that facilitate early diagnosis of the disorder.[20]​.

The largest GWAS study to date was conducted by Dous et al.,[20]​ which analyzed 51,800 participants (21,513 men, 30,287 women) who answered "yes" to the question "Have you been diagnosed with dyslexia?" (who are considered cases) and 1,087,070 participants (446,054 men, 641,016 women) who answered "no" to this question (who are considered controls).

After genotyping these patients and performing the GWAS study, 42 significantly genomic loci broadly associated (P<5x) with dyslexia were identified (which are represented in the Manhattan Diagram of Fig. 1). Additionally, 64 loci with suggestive significance (P<1x) were found.

Of these 42 genomic loci obtained, 17 have already been previously described in the literature, and of these, 15 are associated with cognitive and educational traits. Regarding these identified genes, the following stand out:

• - Gene AUTS2: has been linked to autism and intellectual disability. The variant discovered (rs3735260) represents the strongest AUTS2 SNP association identified with a neurodevelopmental trait to date. This gene has a fundamental role in neurodevelopment and in the migration processes of neurons.

• - Gene TANC2: has been linked to language delay and intellectual disability. This gene controls the connections between brain cells.

• - Gene GGNBP2: has been linked to neurodevelopmental delay and autism. This gene is required for the synaptic development of motor neurons.

The remaining 27 loci have not yet been described in the literature and were therefore considered new. These 27 loci are detailed in the following table:

However, because dyslexia is more prevalent in young people (5.34% in people aged 20 to 30 years) than in adults (3.23% in people aged 80 to 90 years), an additional age- and sex-specific GWAS study was carried out. The results of these subsample analyzes showed a high relationship with the main GWAS. To compare both GWAS (the main one and the age-sex-specific one), they estimated the genetic correlation between sexes and between ages using the linkage disequilibrium score (LDSC) regression method. The genetic correlation between sexes gave a value of 0.91; and the genetic correlation between young people and adults gave a value of 0.97. These values ​​indicate a strong genetic concordance in dyslexia between different groups.

Regarding the GWAS carried out in women, 17 significant genetic variants were identified. Most of these variants (13 of 17) were also significant in the main GWAS. However, four variants (rs61190714, rs4387605, rs12031924, and rs57892111) were not significant in the main GWAS. An intergenic SNP (rs57892111) was also obtained, located between the TFAP2B and PKHD1 genes, which was not significant in the main analysis and has no evidence of association with other human traits in previous GWAS studies. This suggests that these variants could be specific to the female sex. The Manhattan diagram obtained in this female-specific GWAS study can be seen represented in Fig. 2..

Regarding the GWAS performed in men, 6 significant genetic variants were identified (present in the genes CADM2, STAG1, PET112, IER5L, DNMT3B and ARFGEF2). These variants were also significant in the main GWAS, so no specificity was observed in the male sex.

With respect to the regions where these genetic variants are found, the following stand out:

• - Variants in introns: 61% of the genetic variants.

• - Variants in non-coding transcripts: 10% of the genetic variants.

• - Variants in downstream genes: 8% of the genetic variants.

• - Variants in upstream genes: 7% of genetic variants.

• - Variants in intergenic regions: 3% of genetic variants.

Regarding the types of mutations that occur, the following stand out:

• - Nonsense mutation: 55% of genetic variants.

• - Synonymous mutation: 29% of genetic variants.

• - STOP codon gain mutation: 11% of genetic variants.

• - STOP codon loss mutation: 2% of genetic variants.

• - Frameshift mutation: 2% of genetic variants.

The heritability of the SNPs was estimated using the linkage disequilibrium score (LDSC) regression method, obtaining a value of =0.152, considering a prevalence of 5%; and =0.189, considering a prevalence of 10%.

Heritability of dyslexia SNPs showed significant enrichment in conserved regions as well as in H3K4me1 clusters and in genes expressed in frontal cortex, cortex and anterior cingulate cortex. However, no specificity was observed for any type of brain cell (neuron, astrocyte or oligodendrocyte). These findings support the crucial importance of the brain and specific brain regions in the development of dyslexia.

Since reading is a uniquely human trait, it was thought that evolutionary changes in the human lineage would influence the genetic architecture of reading ability. However, no enrichment of significant associations was found for annotations covering different periods of hominid prehistory.

During the study, they attempted to relate the genetics of dyslexia to 98 traits or genetic characteristics, including measures of reading and spelling, hearing difficulties, pain threshold, volumes of subcortical brain structures, surface area and cortical thickness, among others. Of these 98 traits studied, 63 showed significant genetic correlations with dyslexia, which we can see represented in Fig. 3. This suggests that there is a common genetic basis between these traits and dyslexia. Next, we see the most relevant associated characteristics:

• - Quantitative measures of reading and spelling: A negative genetic correlation was observed, meaning that as genes associated with dyslexia increase, reading and spelling skills tend to decrease.

• - Verbal reasoning and numerical reasoning: a negative genetic correlation was observed, which suggests that the greater the genetic risk, the lower your ability to understand and reason using concepts framed in words (verbal reasoning) and the lower your ability to understand the main components that involve a mathematical problem.

• - Intracranial volume: a negative genetic correlation was observed, which means that as intracranial volume decreases, the prevalence of dyslexia tends to increase. No evidence has been found that common genetic variations associated with dyslexia are linked to differences in brain structure, such as subcortical volumes or structural connectivity, in adults. Therefore, the phenotypic correlations observed between dyslexia and brain characteristics may be largely due to environmental factors, possibly related to reading.

• - Attention deficit hyperactivity disorder: a positive genetic correlation was observed, suggesting a genetic connection between dyslexia and ADHD.

• - Ambidextrous: a positive genetic correlation was observed, indicating that there is a genetic correlation between equal use of both hands and being dyslexic.

• - Hearing difficulties: a positive genetic correlation was observed, suggesting that hearing problems at an early age could affect the acquisition of phonological processing skills.

• - Pain threshold: a positive genetic correlation was observed, which could indicate a genetic connection between the experience of pain and dyslexia.

Finally, in this study the Polygenic Risk Score (PGS) of each variant obtained in the GWAS study was calculated. In general, higher PGS scores were observed to be associated with lower reading and spelling accuracy. Thus, PGS were correlated with poorer performance on reading and spelling tests in population-based and enriched samples with reading disorders, especially in made-up word reading, a measure of phonological decoding typically impaired in dyslexia. Therefore, PGS could become a valuable tool to identify children with a propensity for dyslexia, allowing educational support before the development of reading skills.

Future Perspective

The genetic variants identified in this study provide a strong foundation for future research to develop specific biomarkers associated with dyslexia. These biomarkers could become key tools for the early detection of dyslexia in individuals, facilitating more effective interventions and educational supports from the initial stages of development. By better understanding the genetic basis of dyslexia, it opens the door to more precise and personalized diagnostic strategies, which could significantly improve the quality of life of affected individuals by enabling targeted educational interventions and adaptations.

• - Annex: Language disorders.

• - Aphasia.

• - Agraphia.

• - Dyscalculia.

• - Lapses.

• - Easy reading.

• - Andalusian Dyslexia Association (s.f). Positive dyslexia.

• - Angulo Domínguez, M. C., et al. (2010). Manual for attention to students with specific educational support needs derived from specific learning difficulties: DYSLEXIA. Junta de Andalucía. Available at: http://www.juntadeandalucia.es/educacion/webportal/ishare-servlet/content/a9327d5e-1443-445e-9d32-18953f54684f.

• - International Observatory of Dyslexia and other Specific Learning Difficulties.

• - International Organization Dyslexia and Family.

• - Association that works to promote web accessibility for people with dyslexia.

• - Dyslexia: what it is, symptoms, types and exercises for people with dyslexia.

First distinction

Some authors distinguish between the concepts of acquired dyslexia, evolutionary dyslexia and reading delay.

Acquired dyslexia is that which occurs after a specific brain injury, while developmental dyslexia is that which appears in patients who inherently have difficulties in achieving correct reading skills, for no apparent reason to explain it. For its part, reading delay is a reading disorder motivated by specific causes: superficial reading, poor schooling, etc.

Another very important distinction confirmed by Bowers and Wolf (1999, 2000) is a consequence of a known but sometimes ignored fact: not all people improve with the same treatment (traditionally associated with a phonological deficit), even within an apparently homogeneous group of dyslexics (developmental dyslexics, for example). This is because dyslexia can have its origin either in a phonological deficit or in a slow processing speed (the latter individuals have problems decoding many types of information, not just written text). A third type would be the "double deficit." The latter have the greatest reading problems, since they combine both phonological and processing speed problems.

Depending on the type of predominant symptom

1. Superficial dyslexia: is one in which the subject predominantly uses the phonological route. The phonological route is one that allows us to read regular words from smaller segments (syllables). However, subjects with this type of dyslexia will have problems in those words whose writing does not directly correspond to their pronunciation (homophones); This situation occurs mainly with Anglicisms such as hall, thriller or bestseller..

In Spanish, these words are rare (hello, wave) because it is a transparent language (transparent languages are those in which a grapheme can only correspond to one phoneme; that is, writing always corresponds directly and univocally with pronunciation)... except for all those silent "U" that are written next to "g" and "q", and the phonemes represented by more than one letter g/j, k/c/qu, ll/y, b/v, or c/z. They make errors of regularization, repetition, rectification, hesitation, syllabification and accentuation errors, with slow reading. They do not have difficulty reading pseudowords.

2. Phonological dyslexia: it is one in which the subject predominantly uses the visual route to read words. The visual route is one that allows us to read known words globally (without dividing the word into parts). This leads to difficulties in all those unknown or invented words. Lexicalization errors (lobo/lopo), derivational errors (calculator/calculate) and visual errors (pear/pena) are made. They have a longer reaction time when reading pseudowords, while at the same time they have difficulty reading them.

This classification comes mainly from studies with an English-speaking population. English is a very non-transparent language, in which having superficial dyslexia makes the reading and writing processes very difficult. However, dyslexia of this type in the Spanish population would have hardly any consequences on the subject's daily life and would be difficult to diagnose.

This could explain the existence of studies that relate a prevalence of dyslexia to the non-transparency of a language: the spelling of a language would not mean that there were more or fewer dyslexics (which would go against the genetic hypothesis of the disorder), but rather it would make it easier for those cases of predominantly superficial dyslexia to be diagnosed, which would not occur in populations with transparent languages.

Other disorders in specific learning difficulties (SLD) associated with dyslexia

• - Agraphia: disorder related to writing.

• - Dyscalculia: disorder related to arithmetic skills.

• - Dysmapia"): difficulty reading maps and finding places, related to confusion of cardinal points or spatial orientation.

• - Dysperflexia"): moderate aphasia that covers a spectrum of disorders.

• - ADHD: attention deficit hyperactivity disorder.

• - Dysgraphia: specific difficulty in learning to write correctly.

• - Dysphasia: lack of coordination of words.

• - Dyspraxia: lack of coordination in movements.

• - Emotional and behavioral disorders.

Depending on the time of diagnosis

1. • Specific dyslexia: which manifests itself in the period of learning to read.

2. • Comprehension dyslexia: which manifests itself in periods after learning to read and does not allow optimal understanding of what they read.

An objection to this classification would be that comprehension dyslexics may be nothing more than undiagnosed specific dyslexics. It could be that due to different causes, such as, for example, high intelligence, they had compensated or masked their disorder until the increasing demand for understanding academic texts had revealed their disorder.

Neurolinguistics and language psychology are responsible for studying dyslexia.

The applied science that studies its treatment is psychopedagogy.

The professionals who study it are normally graduates specialized in brain and learning, such as neuropsychologists and learning psychologists/psychopedagogues (psychopedagogy).

The treatment of dyslexia must be carried out by specialized professionals, such as neuropsychologists and psychopedagogues, speech therapists (speech therapy) or teachers specialized in learning disorders.

Age at diagnosis and duration of disorder

The signs of dyslexia may vary as the child grows.[9]​.

In general, these disorders are observed for the first time when the subject is learning to read, although they may be latent long before.[10]​ At the same time, it may happen that dyslexia is not diagnosed until many years later. For example, it is common for children who have a high IQ to compensate for this pathology and it goes unnoticed until the comprehension demands increase at school.

There is debate about whether the disorder lasts a lifetime and only its consequences are minimized or whether it disappears thanks to treatments. However, there is agreement that the sooner rehabilitation work begins, the fewer the consequences will be.

Evolutionary course

From 3 to 5 years old, dyslexic children may have slow speech development and pronunciation difficulties, although there do not always have to be difficulties related to oral language.

Some authors also claim that difficulties may appear in learning routines and memorizing numbers, letters, days of the week, songs or colors; difficulties with handling their clothing (buttoning or zipping), etc. However, there is controversy about whether this is more typical of dyslexia or other learning disorders, such as, for example, teachers specializing in therapeutic pedagogy or hearing and language.

In this period it is important to observe how the literacy learning requirements are met. Despite this, it is rare to diagnose dyslexia subjects before the beginning of school, as they have only faced reading tasks.

Between 6 and 8 years old, the biggest complication they present is in the grapheme-phoneme (letter-sound) association.

Other difficulties that appear more rarely in the literature are difficulties in spatial logic operations and in sequential memory.

In some cases, deficits begin to appear in other academic areas, such as mathematics (dyscalculia). In most cases, this dyscalculia is not primary, but is due to difficulties in understanding the problem statements.

In this same age range and up to approximately 11 years old, the child can confuse numbers, letters or change their order in words; He has difficulties in pronouncing the words he reads and has difficulty understanding the readings.

Later and until adulthood, the most important difficulties appear in the comprehension of texts and are greater the more complex the text read.

Cognitive explanation of the symptomatological evolution

From the psychological paradigm of information processing, these difficulties are explained because people without dyslexia automate processes that people with the disorder have difficulty automating.

For these theories, the brain has limited processing capabilities and, if these are exceeded, processes slow down or even errors are made. That is why young children read slowly, make errors in grapheme-phoneme (letter-sound) decoding and have great difficulties in understanding. Furthermore, they have more difficulties with less known or longer words because they require more cognitive resources.

Subsequently, as children automate the reading mechanics, they have more and more resources to dedicate to understanding the text; and finally even this is largely automated.

In subjects with dyslexia, this automation occurs to a lesser extent, so they make errors for much longer, and even as adults, when at first glance the speed and precision of the reading mechanics seem correct, they have comprehension difficulties as they continue to use most of their resources in grapheme-phoneme decoding. Likewise, it is common for adults with dyslexia to continue making more errors and to be slower than the control groups in reading invented or unusual words.

Specific characteristics of dyslexia

There are certain characteristics that always occur and that need to be observed spatially:[11]​.

• - Difficulties in written language.

• - Difficulties in writing.

• - Serious difficulties with spelling.

• - Slow learning to read.

• - Difficulties in learning and writing second languages.

On the other hand, often the following may occur:

• - Difficulties in mathematics.

• - Difficulty following instructions and complex sequences of tasks.

• - Problems understanding written texts.

• - Very significant fluctuations in capacity.

Sometimes they can occur depending on the type of dyslexia or how it has affected the person:

• - Difficulties in spoken language.

• - Problems with the perception of distances and space.

• - Confusion between right and left.

• - Problems with rhythm and musical languages.

Contenido

Tiempo atrás, el tratamiento de la dislexia se anclaba en la idea del refuerzo del área de lateralidad, la orientación espacial, la grafomotricidad, la orientación temporal y las seriaciones. Sin embargo, este tipo de tratamientos están prácticamente abandonados hoy en día.[12]​.

Existe en la actualidad gran cantidad de material específico para prevenir la dislexia, entendido este como un recopilatorio de ideas para mejorar su práctica docente. Entre ellas cabe destacar el uso de los materiales elaborados por el profesor, contribuyendo de esta manera a la enseñanza más individualizada que necesitan los alumnos con rasgos disléxicos.[13]​[13]​[14]​[15]​ Dicho material específico suele estructurarse en orden de dificultad y también por edades.[16]​.

General instructions

A maxim that should guide treatment is "overlearning." That is, relearning reading and writing, but adapting the pace to the child's possibilities.

We must also take into account that both at school and at home, for a dyslexic child, schoolwork will take up more time and effort than for any other child, which sometimes turns it into arduous and tiresome work and, therefore, a task that causes frustration and rejection.

Therefore, in re-education it is important to find activities that are motivating for the child, bringing them closer to reading and writing in a more playful way.

Furthermore, the treatment will depend on the age and developmental stage of the child. The need for this differentiated treatment is closely linked to the changes in the course of the disorder.

According to age

In childhood it will be essential to influence reading requirements in a preventive manner and, consequently, on all children. Among all of them, increasing phonological awareness will be key. For this, oral materials will be used (reading has not yet begun), in which children will have to create rhymes, derive words, divide words into syllables, etc.

Between ages 7 and 10, the objectives will be, on the one hand, to increase phonological awareness, both oral and written; and on the other hand, improve the automation of reading mechanics. For the first, resources similar to those of the previous stage will be used; For the second, we will try to get the child to practice reading aloud as much as possible.

Both at this time and in subsequent times, it is essential that the subject read as much as possible as a way to improve their skills. However, this is not an easy task, since reading can be an exhausting and unpleasant task for a child or adult with dyslexia.

Therefore, it will be essential to find texts appropriate to the age and interests of the subject and motivate them so that reading is an attractive activity. Along these lines, it will also be essential to make parents and teachers of these ages aware of the child's difficulties, so that they are not pushed beyond their capabilities or feel inferior to their peers.

From the age of 10 it has been proven that it is difficult to increase phonological awareness and automation of reading. From this moment, the objectives will be different, fundamentally seeking to teach text comprehension strategies (keyword search, underlining, summary, etc.).

Compensation strategies

It will be in the last stage (from the age of 10) when it will be interesting to propose compensation strategies for the deficits, as a complement to rehabilitation. Compensation strategies are all those that, without modifying the subject's deficient abilities, facilitate their adaptation to daily life by relying on their strengths.

Some helpful instruments may be calculators, voice recordings, data tables or the presence of an adult helping with the oral reading of the study material.

Word processors are also interesting by instantly correcting many of the spelling mistakes and assisting in writing with the support of personalized and themed dictionaries that suggest words.

Controversial therapies

There are many therapies that ensure quick or almost miraculous cures; that enjoy great diffusion in the world; and yet they do not have studies that sufficiently support their usefulness or that they are even discouraged.

The following therapies are at best currently not sufficiently supported by scientific studies; In other cases they start from assumptions that do not agree with the current knowledge of dyslexia.

Before deciding on a treatment, it seems essential to find out from reliable sources whether its effectiveness has really been proven.

Text modified from Journal of Neurology; 2000; 31 (4).

1. • Optometric visual training (optometry): it is based on the theory that dyslexia is due to a visual defect and consists of visual tracking exercises, binocular control, etc. A clear and defined position regarding the non-use of visual training beyond the management of basic visual dysfunction was expressed in a joint statement issued by the Committee on Children with Disabilities, of the American Academy of Pediatrics and an ad hoc working group of the American Association of Pediatric Ophthalmology and Strabismus and the American Academy of Ophthalmology.

2. • Colored lenses: it is based on Irlen's theories and although this method has enjoyed great publicity since the 1980s as a treatment for dyslexia, there are not enough scientific studies to prove its effectiveness.[17]​[18]​.

3. • Cerebellar-vestibular training: it is based on theories that affirm that the underlying problem of dyslexia is actually a problem of the cerebellum and the ear (balance centers); and consists mainly of exercises aimed at improving stability, or antivertigo drugs. There is no evidence to support either this theory or the treatments it proposes.

4. • Sensory integration therapy: is based on the theory that learning problems and motor problems are due to a sensory integration deficit. Its ineffectiveness has been proven compared to other intervention programs.

5. • Electroencephalographic feedback (EEG Biofeedback): it is based on the assumption that both in dyslexia and in other disorders (for example, attention deficit/hyperactivity) there is an abnormal underlying brain functioning. Thus, the defenders of this therapy consider that if the electroencephalographic patterns are modified, the external difficulties will also be modified. In addition to its high cost, the studies that have reported its usefulness so far are inadequate from a methodological point of view. The groups were small and without appropriate controls.

La dislexia es un trastorno altamente poligénico con una arquitectura genética compleja. Estudios familiares han estimado que este trastorno presenta una heredabilidad del 70%.[19]​ Por lo tanto, actualmente, las investigaciones en el campo de la dislexia buscan identificar los factores de riesgo genético asociados con esta condición. Estos esfuerzos no solo contribuirán a mejorar la comprensión de los mecanismos biológicos que subyacen a esta enfermedad, sino que también podrían mejorar las técnicas de diagnóstico, permitiendo la identificación temprana de personas susceptibles a la dislexia.[20]​.

GWAS studies

With the aim of studying these genetic risk factors associated with dyslexia, numerous genome-wide association studies (GWAS) have been carried out on the genome of patients to better understand the genetic component of this disease and design new biomarkers that facilitate early diagnosis of the disorder.[20]​.

The largest GWAS study to date was conducted by Dous et al.,[20]​ which analyzed 51,800 participants (21,513 men, 30,287 women) who answered "yes" to the question "Have you been diagnosed with dyslexia?" (who are considered cases) and 1,087,070 participants (446,054 men, 641,016 women) who answered "no" to this question (who are considered controls).

After genotyping these patients and performing the GWAS study, 42 significantly genomic loci broadly associated (P<5x) with dyslexia were identified (which are represented in the Manhattan Diagram of Fig. 1). Additionally, 64 loci with suggestive significance (P<1x) were found.

Of these 42 genomic loci obtained, 17 have already been previously described in the literature, and of these, 15 are associated with cognitive and educational traits. Regarding these identified genes, the following stand out:

• - Gene AUTS2: has been linked to autism and intellectual disability. The variant discovered (rs3735260) represents the strongest AUTS2 SNP association identified with a neurodevelopmental trait to date. This gene has a fundamental role in neurodevelopment and in the migration processes of neurons.

• - Gene TANC2: has been linked to language delay and intellectual disability. This gene controls the connections between brain cells.

• - Gene GGNBP2: has been linked to neurodevelopmental delay and autism. This gene is required for the synaptic development of motor neurons.

The remaining 27 loci have not yet been described in the literature and were therefore considered new. These 27 loci are detailed in the following table:

However, because dyslexia is more prevalent in young people (5.34% in people aged 20 to 30 years) than in adults (3.23% in people aged 80 to 90 years), an additional age- and sex-specific GWAS study was carried out. The results of these subsample analyzes showed a high relationship with the main GWAS. To compare both GWAS (the main one and the age-sex-specific one), they estimated the genetic correlation between sexes and between ages using the linkage disequilibrium score (LDSC) regression method. The genetic correlation between sexes gave a value of 0.91; and the genetic correlation between young people and adults gave a value of 0.97. These values ​​indicate a strong genetic concordance in dyslexia between different groups.

Regarding the GWAS carried out in women, 17 significant genetic variants were identified. Most of these variants (13 of 17) were also significant in the main GWAS. However, four variants (rs61190714, rs4387605, rs12031924, and rs57892111) were not significant in the main GWAS. An intergenic SNP (rs57892111) was also obtained, located between the TFAP2B and PKHD1 genes, which was not significant in the main analysis and has no evidence of association with other human traits in previous GWAS studies. This suggests that these variants could be specific to the female sex. The Manhattan diagram obtained in this female-specific GWAS study can be seen represented in Fig. 2..

Regarding the GWAS performed in men, 6 significant genetic variants were identified (present in the genes CADM2, STAG1, PET112, IER5L, DNMT3B and ARFGEF2). These variants were also significant in the main GWAS, so no specificity was observed in the male sex.

With respect to the regions where these genetic variants are found, the following stand out:

• - Variants in introns: 61% of the genetic variants.

• - Variants in non-coding transcripts: 10% of the genetic variants.

• - Variants in downstream genes: 8% of the genetic variants.

• - Variants in upstream genes: 7% of genetic variants.

• - Variants in intergenic regions: 3% of genetic variants.

Regarding the types of mutations that occur, the following stand out:

• - Nonsense mutation: 55% of genetic variants.

• - Synonymous mutation: 29% of genetic variants.

• - STOP codon gain mutation: 11% of genetic variants.

• - STOP codon loss mutation: 2% of genetic variants.

• - Frameshift mutation: 2% of genetic variants.

The heritability of the SNPs was estimated using the linkage disequilibrium score (LDSC) regression method, obtaining a value of =0.152, considering a prevalence of 5%; and =0.189, considering a prevalence of 10%.

Heritability of dyslexia SNPs showed significant enrichment in conserved regions as well as in H3K4me1 clusters and in genes expressed in frontal cortex, cortex and anterior cingulate cortex. However, no specificity was observed for any type of brain cell (neuron, astrocyte or oligodendrocyte). These findings support the crucial importance of the brain and specific brain regions in the development of dyslexia.

Since reading is a uniquely human trait, it was thought that evolutionary changes in the human lineage would influence the genetic architecture of reading ability. However, no enrichment of significant associations was found for annotations covering different periods of hominid prehistory.

During the study, they attempted to relate the genetics of dyslexia to 98 traits or genetic characteristics, including measures of reading and spelling, hearing difficulties, pain threshold, volumes of subcortical brain structures, surface area and cortical thickness, among others. Of these 98 traits studied, 63 showed significant genetic correlations with dyslexia, which we can see represented in Fig. 3. This suggests that there is a common genetic basis between these traits and dyslexia. Next, we see the most relevant associated characteristics:

• - Quantitative measures of reading and spelling: A negative genetic correlation was observed, meaning that as genes associated with dyslexia increase, reading and spelling skills tend to decrease.

• - Verbal reasoning and numerical reasoning: a negative genetic correlation was observed, which suggests that the greater the genetic risk, the lower your ability to understand and reason using concepts framed in words (verbal reasoning) and the lower your ability to understand the main components that involve a mathematical problem.

• - Intracranial volume: a negative genetic correlation was observed, which means that as intracranial volume decreases, the prevalence of dyslexia tends to increase. No evidence has been found that common genetic variations associated with dyslexia are linked to differences in brain structure, such as subcortical volumes or structural connectivity, in adults. Therefore, the phenotypic correlations observed between dyslexia and brain characteristics may be largely due to environmental factors, possibly related to reading.

• - Attention deficit hyperactivity disorder: a positive genetic correlation was observed, suggesting a genetic connection between dyslexia and ADHD.

• - Ambidextrous: a positive genetic correlation was observed, indicating that there is a genetic correlation between equal use of both hands and being dyslexic.

• - Hearing difficulties: a positive genetic correlation was observed, suggesting that hearing problems at an early age could affect the acquisition of phonological processing skills.

• - Pain threshold: a positive genetic correlation was observed, which could indicate a genetic connection between the experience of pain and dyslexia.

Finally, in this study the Polygenic Risk Score (PGS) of each variant obtained in the GWAS study was calculated. In general, higher PGS scores were observed to be associated with lower reading and spelling accuracy. Thus, PGS were correlated with poorer performance on reading and spelling tests in population-based and enriched samples with reading disorders, especially in made-up word reading, a measure of phonological decoding typically impaired in dyslexia. Therefore, PGS could become a valuable tool to identify children with a propensity for dyslexia, allowing educational support before the development of reading skills.

Future Perspective

The genetic variants identified in this study provide a strong foundation for future research to develop specific biomarkers associated with dyslexia. These biomarkers could become key tools for the early detection of dyslexia in individuals, facilitating more effective interventions and educational supports from the initial stages of development. By better understanding the genetic basis of dyslexia, it opens the door to more precise and personalized diagnostic strategies, which could significantly improve the quality of life of affected individuals by enabling targeted educational interventions and adaptations.

• - Annex: Language disorders.

• - Aphasia.

• - Agraphia.

• - Dyscalculia.

• - Lapses.

• - Easy reading.

• - Andalusian Dyslexia Association (s.f). Positive dyslexia.

• - Angulo Domínguez, M. C., et al. (2010). Manual for attention to students with specific educational support needs derived from specific learning difficulties: DYSLEXIA. Junta de Andalucía. Available at: http://www.juntadeandalucia.es/educacion/webportal/ishare-servlet/content/a9327d5e-1443-445e-9d32-18953f54684f.

• - International Observatory of Dyslexia and other Specific Learning Difficulties.

• - International Organization Dyslexia and Family.

• - Association that works to promote web accessibility for people with dyslexia.

• - Dyslexia: what it is, symptoms, types and exercises for people with dyslexia.