Down syndrome is a chromosomal condition caused by a cell division error. The error leads to the creation of an additional chromosome 21. This condition alters the physical growth and cognitive ability of the affected individuals ( Bittles et al., 2007; Leshin, 2003 ). It also causes developmental challenges while increasing the risk of other health problems. Down syndrome can be detected either before or after birth. Several tests and screenings have to be carried out to facilitate detection. Down syndrome is caused by a series of factors, and the likelihood of occurrence increases with age ( Leshin, 2003) . Down syndrome should not be considered an illness. Instead, the term is descriptive of the features that arise as a result of the changes taking place. This paper will examine Down syndrome, its implications on mental health, and its effects on the affected person’s brain.
Down Syndrome: A Background
Usually, each cell in the human body has 46 chromosomes, with each parent contributing half the number. Down syndrome occurs when all or a significant number of an individual's cells feature an extra copy of chromosome 21 ( Bittles et al., 2007; Leshin, 2003 ). Persons with this condition often have very distinct physical characteristics, varied cognitive development, and unique health-related issues. Down syndrome is best recognized through the victims’ eyes. Specifically, the eyes slant upwardly, the iris has white spots, oblique fissures appear, while epicanthic skin folds appear on the eyes’ inner corners ( Leshin, 2003) . Those with Down syndrome boast a low muscle tone, flat nasal bridge, protruding tongue, short neck, small stature, and deep creases at the center of their palms. The large and second fingers have more space between them, while the fifth finger has one flexion furrow.
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There are different types of Down syndrome. The most common form is referred to as trisomy 21 ( Bittles et al., 2007; Leshin, 2003 ). Each cell in individuals with trisomy 21 has 47 chromosomes as opposed to 46. An error, also referred to as non-disjunction, is responsible for trisomy 21 and takes place at or before conception. On occurring, the error leaves an egg cell or sperm cell with an additional copy of chromosome 21. Up to 95% of all cases of Down syndrome are as a result of this error, while 5% are as a result of translocation and mosaicism ( Leshin, 2003 ). The mosaic form of the syndrome is manifested when some cells in an individual's body have trisomy 21, while others are normal. On the other hand, Robertsonian translocation takes place due to breaking off of a part of chromosome 2 during the process of cell division. Subsequently, the broken part attaches itself to a different chromosome, in most cases, chromosome 14. It is this additional part of chromosome 21 that leads to the development of features related to Down syndrome ( Leshin, 2003) . Often, an individual in which translocation occurs rarely has unique physical attributes. However, such an individual is likely to give birth to a child who boasts an additional chromosome 21. Individuals with Down syndrome often exhibit cognitive development profiles that are suggestive of intellectual disability that is mild or moderate. Children who have Down syndrome are likely to delay reaching critical developmental milestones compared to their counterparts in the same age group ( Leshin, 2003 ). For instance, a child may delay learning how to talk. When this happens, such a child may be forced to go for speech therapy in a bid to help him or her obtain expressive language. The child may also exhibit delayed fine motor skills that may occur even after the child has acquired gross motor skills. A child suffering from Down syndrome experiences delays sitting, crawling, and even walking. The child also experiences challenges related to attention, impulsive behavior, and making judgments ( Leshin, 2003) . It is worth noting that these shortcomings cannot prevent affected children from attending a school or contributing to their communities.
Individuals with Down syndrome may also exhibit general health challenges that are likely to affect different bodily functions and organ systems. For instance, a significant percentage of those with Down syndrome are likely to have congenital heart defects. They also have an increased risk of hearing problems, epilepsy, Alzheimer's disease, respiratory challenges, thyroid issues, and leukemia ( Paladini et al., 2000 ).
Mental State of Down Syndrome
Up to half of all adults and children with Down syndrome are confronted by a major issue related to their mental health in their lifetime. Those with numerous medical challenges are even more likely to experience mental health challenges at a higher rate. The most prevalent mental health issues related to Down syndrome include depression, anxiety, impulsive and oppositional behaviors, obsessive-compulsive and repetitive behaviors, neuropsychological problems, decline in cognitive skills, and autism spectrum disorders (ASD) ( Määttä et al., 2006 ). The pattern of manifestation of mental health challenges in Down syndrome differs from individual to another based on each person’s developmental characteristics and age.
Anxiety is the most common of all the mental health issues related to Down syndrome in both adults and children. The two most notable forms of this anxiety are situational and baseline anxiety ( Chundamala et al., 2009 ). However, each type of anxiety has its own set of stressors. Situational anxiety becomes more profound when an individual is anticipating new situations as well as during transitions. In children, the latter can either be taking place in school or at home. They also could be associated with such times as bedtime or mealtime. Other scenarios include being in unfamiliar situations whereby the environment results in uncertain expectations.
The elevated levels of worry and restlessness associated with obsessive-compulsive behavior may cause an adult or child to become rigid. When rigidity happens, the individual in question ought to follow familiar routines. Also, the individual may engage in repetitive and ritualistic behavior. In such circumstances, the individual with Down syndrome is likely to be either fearful or unhappy. Often, the two mental states of obsessive-compulsive behaviors and anxiety co-exist ( Määttä et al., 2006 ). Also, as opposed to being unhappy, the inattentive, disruptive, and oppositional child with Down syndrome is likely to be excited and happy. The nature of the issues that manifest in individuals with Down syndrome makes the work of caregivers a bit challenging. This is because such persons are often stuck, which results in increased negative attention.
In young children with Down syndrome, the symptoms of attention deficit hyperactivity disorder (ADHD) and those of anxiety have to be differentiated. The compulsiveness, fidgeting, and restlessness that are associated with a condition of generalized anxiety have an easily identifiable onset and follow an intermittent course. This phenomenon contrasts the behavior of adults and children with an attention-deficit, oppositional, and impulsive profile. Therefore, a detailed history of all situations must be taken for ease of identification of the environmental triggers of anxiety. Notable triggers include changes in immediate work, school, or home environments ( Määttä et al., 2006). In such scenarios, it is essential that behavioral-modification, as well as management plans, are put in place. Also, there is a need to assess the antecedents, behaviors, and consequences (ABCs). While anti-anxiety medications or antidepressants are helpful, their use should be reserved for use in dealing with more severe and persistent levels of the identified symptoms.
Both adults and children that show depressive symptoms also display signs of extreme social withdrawal, reduced ability to enjoy activities that they previously used to enjoy, and increased sad feelings. Both caregivers and parents confirm that such signs indicate a significant change from the individuals' past demeanor. Individuals suffering from anxiety or depression experience disrupted sleep, which makes it difficult for them to distinguish between the two states clearly. One element of depression in individuals with Down syndrome is that it is closely associated with toxic environmental triggers ( Sherman et al., 2007). Examples of these triggers include previous medical illnesses that had not been discovered, psychosocial stressors such as separation from an older sibling once the latter moves to college, chronic or sudden diseases, absence of a favorite teacher, or death of a pet. These events, according to adults and children with Down syndrome, are not ordinary. The events also bear a psychological impact that is disproportionate when compared to the response that a normal person gives when faced with the same circumstances.
Effects of Down Syndrome on the Brain
The accurate coordination of communication between an extensive network of nerve cells is required for the comprehensive processing of information in the human brain. The nerve cells are firmly wired together in electrical circuits using junctions that are referred to as synapses. In an individual with Down syndrome, abnormal function, and structure of synapses is exhibited in the networks of the brain's hippocampus ( Hanson et al., 2007 ). The hippocampus acts as the center for memory and learning, allowing individuals to integrate their past experiences with their present contexts. These functions are made possible by place cells. By forming maps of an individual's environment, place cells play the role of the brain's GPS.
The dysfunction exhibited at the hippocampus' input synapses propagates around the hippocampal circuits in individuals with Down syndrome. This destabilizes the processing of information by place cells and impairs memory and learning. As an individual grows old, similar impairments, irrespective of degree, have an unprecedented impact on the individual’s intellectual capacities ( Netzer et al., 2010 ). The amplified expression of chromosome 21 genes, as exhibited in individuals with Down syndrome makes the hippocampus more vulnerable to dysfunction. Consequently, individuals with Down syndrome experience difficulties with memory and learning, which are the two most essential functions of the brain ( Netzer et al., 2010) . These difficulties may be experienced throughout one’s life and may also trigger cognitive problems later in life. Thus, for any treatment regime to be effective, it has to be backed with a comprehensive, careful, and scientific methodology to understand the causes of cognitive challenges in individuals with Down syndrome.
The additional copy of chromosome 21, as exhibited by individuals with Down syndrome, causes various changes in the brain owing to its regulatory sequences and genes. Therefore, for one to define the cause of brain-related challenges, he or she has to start by identifying the cellular and gene mechanisms that are responsible ( Yizhar et al., 2011 ). However, finding the specific genes responsible and pinpointing the mechanism via which the additional copies of the genes cause the problems might be challenging.
The changes noted in cognition are driven by dysfunction of the brain circuits that enable cognitive function. The efficient operation of these circuits plays a crucial role in determining all brain functions. Therefore, all changes taking place in the brain function are a result of alterations in the circuit function ( Yizhar et al., 2011; Hanson et al., 2007 ). The circuits are comprised of closely connected neurons. Thus, the changes experienced in the brain circuits are likely to be found in the function and structure of neurons, as well as the connections that these neurons make. A synapse, in this case, denotes the points at which neurons communicate with one another. At the synapse, one neuron excites the next one in the circuit resulting in the formation of an excitatory synapse. In an alternative instance, the synapse allows a neuron to hinder the activity of a second neuron, in the process establishing an inhibitory synapse.
The functioning of normal circuits is facilitated by a proper balance between inhibition and excitation ( Yizhar et al., 2011 ). An excess of the former blocks cognitive function while an excess of the latter may result in a seizure. Synaptic changes cannot be decoupled from the disorders associated with brain function such as Down syndrome. Synapses in brain circuits of individuals with Down syndrome exhibit abnormality both in function and structure. Likewise, the spines and synapses that house these circuits are often enlarged, which is indicative of an underlying functional challenge. Excessive inhibition results in an imbalance that subsequently compromises the circuit function ( Yizhar et al., 2011) . This alters the brain circuits affecting their ability to fire as actively as would be expected. Ultimately, this results in the impairment of both memory and learning.
In a bid to restore cognition in individuals with Down syndrome to normal levels, understanding the genes responsible for the imbalance noted in the brain is requisite. This process may require narrowing down these genes as well as how they work. For instance, cognition can be enhanced by interrupting inhibition via a particular class of inhibitory receptors. It is also worth noting that people with Down syndrome form the largest group of individuals with Alzheimer's disease whose cause is genetics ( Hartley et al., 2015) . This is because those with Down syndrome are predisposed to develop Alzheimer's, particularly in their middle age. The gene most commonly associated with this is the Amyloid Precursor Protein (APP), which resides in chromosome 21. The additional copy of APP in individuals with Down syndrome plays a crucial role in the demise of neurons in older individuals, which results in the manifestation of Alzheimer's disease.
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