Development of the Prefrontal Cortex in Males

Overview

The prefrontal cortex (PFC) is located in the front part of the brain just behind the forehead. Responsible for cognitive functions such as abstract thought and the management of attention, problem-solving, and the modulation of intense emotions, the prefrontal cortex is one of the last regions of the brain to develop. MRI studies of the brain have indicated that the brain develops from the front to back, which is why the PFC is the last part of the brain to develop; the development of the PFC is typically done developing at the age 25. Studies have indicated that teenagers have less myelin (white matter) than adults (Zaidi, 2010, p.48). More myelin growth comes as the connections between brain mechanisms are strengthened. 

The growth of white matter in the brain generally happens naturally as connections between the two hemispheres of the brain improve as adolescents continue to engage in abstract thought during complex social situations and dilemmas. Experience plays a foundational role in the development of these connections. While the PFC is still immature, adolescents will typically make irrational and risky decisions because the connections between the hemispheres of the brain are still under development. 

Men versus Women

In both men and women, the PFC is particularly vulnerable to the malign effects of aging. However, men are particularly vulnerable to these effects. Among the many neuro-transmitting systems of the brain, the prefrontal dopaminergic system is especially important because of its role in regulating various cognitive functions. Several studies have documented that aging in males is accompanied by declining functions of the dopaminergic systems. These studies have concluded that, as men age, they are more susceptible to lessened ability to engage in abstract thinking or problem-solving. 

Development of the PFC during Adolescence 

The PFC undergoes significant changes during adolescence, which has been well documented; however, in 2007, the University of Illinois published a study that indicates that neurons in the male, adolescent brain actually die during puberty. This is accelerated with adolescents engaging in substance abuse. The implications of this finding may have a significant impact on what the scientific community understands about male, brain development during adolescence. Moreover, the loss of neurons in the PFC during adolescence may shed light on teenage pathologies like schizophrenia, which typically occurs in late adolescence in males. Although the loss of these neurons in the PFC may be detrimental, Juraska (2007) suggests, we always think that having more neurons is better, and it might not be. In some stages of early child development up to half of the neurons in some brain regions are lost. The pruning away of unneeded or disruptive neural circuits appears to be as important to development as the growing of new neural connections. Although other researchers ha[ve] seen reductions in the size of the cortex, no one thought neurons were lost, unless some terrible thing were happening. Now we are seeing that some major changes are occurring in adolescence that no one has suspected (para 10). Studies such as these highlights the idea there is still so much about the development of the PFC during early and late adolescence. 

While the scientific community unanimously agrees that the PFC undergoes significant development during early adolescence until the age of 25, few studies have explored the development of the PFC in males during the various stages of adolescence. In a study conducted by Ninette Fernandes (2010), she studied two varied groups of male teenagers and adults to examine the varied development of the PFC. She hypothesized that the older group would outperform the younger in a series of tasks. Her testing consistently showed that the older group performed significantly better on tasks that required abstract thinking, planning, decisions making, and memory. Furthermore, Fernandes’ study revealed and corroborated past findings related to risk-taking and impulsive behavior in males. In the younger group, subjects were found to perform significantly greater amounts of irrational, quick, and impulsive decisions. This particular finding is important because it suggests that an undeveloped PFC in a male adolescent can affect the ability to make decisions without being impulsive and lead to greater degrees of unnecessary risk-taking. 

Just as important as tracking the development of the male PFC during adolescence and early adulthood is examining the causes that inhibit the development of the PFC. Fernandez (2010) posits, “Human and animal studies have shown the PFC to be sensitive to stress, and this is especially relevant during the transitional period between adolescence and adulthood” (p.33) She distinguishes the effects of short-term and long-term stress as events that occurred in the past year and the stress that has occurred since the age of 11. Her findings suggest that stress experienced over time, in the aggregate, exerts a greater negative impact on the PFC than isolated events that result in negative stress. Fernandes (2007) concludes in her study, 

Overall, the best predictive model of PFC functioning included two predictors: negative stress from the past year and negative stress since the age of 11. In addition to the combined predictive power of these two measures, it appears that negative stress since the age of 11 is an independent, unique, and better predictor of PFC functioning than the negative stress score from the past year (p.102). 

The results of studies similar to this one are important because they can contribute to an effort to assist male adolescents and young adults maximize their potential by mitigating any malignant effects on the development of the PFC. An admitted shortcoming of the studies related to the development of the male PFC is the inability to detect its progress on the margin. For example, studies have failed to identify if the most development of the PFC occurs between 18-20 or 21-23. If these studies could establish time frames such as this, corrective action could be taken to help adolescents avoid behavior that would induce stress. 

Physical Development of the PFC

The PFC develops from the neural tube, which is an embryonic structure that eventually develops in the brain and spinal cord. Requiring over two-decades of maturation, the PFC undergoes one of the longest periods of maturation compared to other regions of the brain. The development of the PFC occurs at the prenatal and childhood years and both stages are defined by significant structural and cognitive changes. Although the changes that occur on these two levels are pronounced, the synthesis of genetic and environmental factors that affect the development of the PFC is still largely unknown. 

Maturation of the male PFC

The development of the male PFC is a complex process that is heavily influenced through genetics, the theory of development, and external environmental factors. Some of the processes that lead to a healthy developed PFC occur during gestation, and others are completed at birth. The “wiring” of the brain that individuals colloquially refer to occurs when neurons fire and create a network as cognitive activities are repeatedly engaged in. The synapses, the connection between neurons, are actually most dense on average at the age of 3.5. The synaptic density will decrease during a process referred to as “pruning” in which unneeded synapses are destroyed to the overall level of adults. This time of development is defined by some much change that male children and adolescents are especially vulnerable to an array of neuropsychiatric disorders, which serves as an explanation as to why mental health professionals often examine the childhood and adolescent periods of a patient’s life to arrive at a diagnosis. 

In order to instigate the growth of the PFC, repeated stimulation of the neurons is needed to engender the growth of synaptic networks. As previously stated, genetic factors play a major role in the development of the PFC; however, environmental factors are equally important to induce such simulation. Male children and adolescents who are encouraged to solve problems, challenged to reason, and participate in varied songs, games, and memory tasks will experience increased neural activity, and, consequently, contribute positively to the development of the PFC (Gao, Wang, Snyder, Li, p.13). On the other hand, children who possess genetic disorders are otherwise unexposed to these cognitive exercises will suffer from an underdeveloped PFC. Diseases related to the development of the male PFC. 

Although mental health disorders encompass a wide range of pathologies with an even wider, overlapping list of symptoms,  male PFC dysfunction is often a symptom or a cause of an overwhelming majority of mental health disorders such as schizophrenia, ADHD, depression, bipolar disorders, anxiety disorders, autism spectrum disorders, obsessive-compulsive disorder, eating disorders, and addictive behaviors. PFC is a symptom of these disorders because most of them are accompanied by an inability to reason, plan, and control impulses. Consequently, further studies that can shed more light on the developmental processes of the PFC can help handle, manage, and minimize the growing number of individual with mental health disorders. 

References

Fernandes, N. (n.d.). THE DETECTION OF PFC DEVELOPMENT. OhioLink. Retrieved March 22, 2013, from http://etd.ohiolink.edu/send-pdf.cgi/Fernandes%20Ninette%20M.pdf?marietta1164924291

Gao, W. J., Wang, H., Snyder, M., & Li, Y. (n.d.). The Unique Properties of the Prefrontal Cortex and Mental Illness. Drexelmed.edu. Retrieved March 23, 2013, from neurobio.drexelmed.edu

Juraska, J. (n.d.). Prefrontal cortex loses neurons during adolescence. EurekAlert! - Science News. Retrieved March 23, 2013, from http://www.eurekalert.org/pub_releases/2007-03/uoia-pcl031307.php

Zaidi, Z. (2010). Gender Differences in Human Brain: A Review. The Open Anatomy Journal, 2, 37-55. Retrieved March 23, 2013, from http://www.benthamscience.com/open/toanatj/articles/V002/37TOANATJ.pdf