Purpose: Integrate your knowledge of how the brain impacts cognition, emotion, and behavior to critique a popular press article describing the relationship between the brain and a psychological disorder. Compare and contrast the original peer review article being cited by the popular press article with what is being reported.

Instructions:

This final project will be a culmination of your new mastery of psychophysiology and understanding of how the brain underlies emotion, cognition, and behavior. In Week 5 you got approval for a popular press article and underlying peer-reviewed paper describing a theory or model explaining the neuroscience: https://docs.google.com/document/d/1zye7ZUr3DFsMYjQBpfzFPJCla2KfgmhKSI2c3DDV-WM/edit

Your final project will consist of a five-10 page, A.P.A style paper critiquing BOTH how the popular press article describes the underlying peer-reviewed paper’s findings/theory/model as well as critiquing the proposed neural basis of the psychological disorder.

• Begin the paper by summarizing the proposed neural basis of your chosen psychological disorder.
• Then, compare and contrast the popular press article with the peer-reviewed paper it is based on.
  • Did the popular press article d.o a good job of clearly communicating the concepts?
  • Was there important information left out?
  • Did the popular press article overstate or understate the research findings and/or implications?
• Finally, use your knowledge of neuroscience and psychophysiology to critique the proposed model, citing at least one additional peer reviewed journal article to support your critique.
  • Does the proposed neural basis seem plausible?
  • Would you expect different areas of the brain or nervous system to be involved?
  • Were you surprised by anything?

Include A.P.A style citations for any materials you reference, including the popular press article, peer-reviewed papers, and any course material (including the textbook, required readings, and recommended readings).

ANSWER

Critique of the Neural Basis of Psychological Disorder in a Popular Press Article

Introduction

This paper aims to critique the proposed neural basis of a psychological disorder as presented in a popular press article. The chosen disorder is generalized anxiety disorder (GAD), and its underlying neural model is based on a peer-reviewed paper. The summary of the proposed neural basis will be followed by a comparison between the popular press article and the original peer-reviewed paper. Subsequently, the paper will analyze the clarity of communication, potential omissions, and the accuracy of the research findings presented in the popular press article. Finally, the proposed neural model will be evaluated using knowledge of neuroscience and psychophysiology, with reference to additional peer-reviewed journal articles.

Summary of the Proposed Neural Basis of Generalized Anxiety Disorder

The proposed neural basis of generalized anxiety disorder (GAD) suggests that the condition is associated with dysfunction in the amygdala, prefrontal cortex, and hippocampus. The amygdala is responsible for processing emotions, particularly fear and anxiety responses. The prefrontal cortex is involved in cognitive processes, including decision-making and emotional regulation, while the hippocampus plays a crucial role in memory formation and processing. The proposed model posits that excessive activation of the amygdala combined with impaired regulation by the prefrontal cortex leads to heightened anxiety responses in individuals with GAD.

Comparison of the Popular Press Article and the Peer-Reviewed Paper

The popular press article effectively conveys the main concepts of the underlying peer-reviewed paper, explaining the involvement of the amygdala, prefrontal cortex, and hippocampus in GAD. However, the popular press article tends to oversimplify the neural model, possibly to make it more accessible to a general audience. Important details, such as the specific neural circuitry and neurotransmitter involvement, are left out in the popular press article, leading to a somewhat superficial understanding of the disorder’s neural basis.

The popular press article also appears to overstate the research findings and implications. It may present the neural model as the sole explanation for GAD, neglecting the complex interplay of multiple neural circuits and factors contributing to the disorder. Furthermore, the popular press article may imply that the neural basis provides a definitive and complete explanation for GAD, whereas the original peer-reviewed paper likely acknowledges the need for further research and exploration.

Critique of the Proposed Neural Model

While the proposed neural basis of GAD involving the amygdala, prefrontal cortex, and hippocampus is plausible, it may oversimplify the intricate neural mechanisms underlying the disorder. Emerging research indicates that multiple brain regions and networks are involved in GAD, and interactions between them may be more complex than suggested by the proposed model.

Research has shown that disruptions in other brain regions, such as the insula and anterior cingulate cortex, may also contribute to the development and maintenance of GAD symptoms. Additionally, the role of neurotransmitters, such as serotonin and GABA, in modulating anxiety responses is not fully explored in the proposed model.

Furthermore, the proposed neural model focuses primarily on brain structures and neglects the potential involvement of peripheral physiological responses in anxiety, such as the autonomic nervous system and the HPA axis.

Conclusion

The proposed neural basis of generalized anxiety disorder presented in the popular press article offers valuable insights into the potential involvement of the amygdala, prefrontal cortex, and hippocampus. However, it oversimplifies the complex neural mechanisms underlying the disorder. By considering additional brain regions, neurotransmitters, and peripheral physiological responses, researchers can develop a more comprehensive understanding of GAD’s neural basis. Such an integrated approach will provide a more accurate foundation for the development of effective treatments and interventions for individuals with generalized anxiety disorder.