The Relation Between A Brain Protein And Depression/Stress/Anxiety
By: Cassandra Portelli
With the ascent of innovation and web-based media, everyone is centred around outside
stimulation and different types of entertainment. In the present atmosphere, students, workers,
and people from all walks of life are stuck most days sitting on a desk looking at their
technological screens. The effect of this new lifestyle has created a rise in mental illness relating
to stress, anxiety, and depression. Can new scientific research create more solutions to this
ongoing problem? In fact, according to Sousa et al. (2020), a study led by researchers at
Karolinska Institutet in Sweden found that the protein p11 deficiency is linked to depression,
stress, and anxiety.
The study led by Sousa et al. (2020) states that the hypothalamic-pituitary-adrenocortical
(HPA) and the sympathetic–adrenal–medullary (SAM) axes are linked to a healthy response to
stress. These systems from the start of humanity evolved as defence mechanisms to cope and
survive in our environment (Sousa et al., 2020). Prolonged stress can lead to depression which
would therefore be manifested as high concentrations of corticotropin-releasing hormone (CRH)
and negatively impact the adrenocorticotropic hormone (ACTH) (Sousa et al., 2020). The
investigation by Sousa et al. (2020) reviewed the p11 expression to HPA and SAM axes limits
by analyzing p11 deficiencies in mice. The mice were tested using behavioural, endocrine, and
physiological readouts and were shown to have a higher heart rate and more anxiety with p11
definciencies (Sousa et al., 2020). In conclusion, p11 affects the initial release of cortisol (stress
hormone) in mice through modulation of specific neurons in the in the nerve centre part of the
brain (Sousa et al., 2020). As well, p11 seems to manage more than one pathway beginning in
the brainstem as it influences the arrival of two different stress hormones, adrenaline and
noradrenaline (Sousa et al., 2020). As per Sousa et al. (2020), the protein p11 directs the HPA
axes through adjustment of cell activity and was found to change the sensitivity of the heart
through 5-HT4 receptors. Most importantly, p11 shortage was found to slow the responsiveness
to antidepressants (Sousa et al., 2020).
The need for the study done by Karolinska Institutet is undeniable. According to Lowe
(2018), Graduate students from all over the world face ongoing amounts of stress and anxiety
and not surprisingly, the rate of students experiencing anxiety goes up each year. Graduate
students are more prone to experiencing depression and anxiety compared to other people
(Evans et al., 2018). Not known to many people, stress is a major contributor to physical
conditions. For example, the effects of stress on bone growth in which impaired bone growth,
specifically the growth plate, is observed in children that undergo stress (Sävendah, 2012).
Furthermore, the study relating to the effects of acute and chronic stress on Diabetes control
(not the cause of Diabetes). Stress can make hormonal changes that can influence glucose
homeostasis in both ordinary individuals and individuals with diabetes and can adversely affect
blood glucose concentrations in patients with type 1 and 2 diabetes (Marcovecchio & Chiarelli,
2012).
By: Cassandra Portelli
With the ascent of innovation and web-based media, everyone is centred around outside
stimulation and different types of entertainment. In the present atmosphere, students, workers,
and people from all walks of life are stuck most days sitting on a desk looking at their
technological screens. The effect of this new lifestyle has created a rise in mental illness relating
to stress, anxiety, and depression. Can new scientific research create more solutions to this
ongoing problem? In fact, according to Sousa et al. (2020), a study led by researchers at
Karolinska Institutet in Sweden found that the protein p11 deficiency is linked to depression,
stress, and anxiety.
The study led by Sousa et al. (2020) states that the hypothalamic-pituitary-adrenocortical
(HPA) and the sympathetic–adrenal–medullary (SAM) axes are linked to a healthy response to
stress. These systems from the start of humanity evolved as defence mechanisms to cope and
survive in our environment (Sousa et al., 2020). Prolonged stress can lead to depression which
would therefore be manifested as high concentrations of corticotropin-releasing hormone (CRH)
and negatively impact the adrenocorticotropic hormone (ACTH) (Sousa et al., 2020). The
investigation by Sousa et al. (2020) reviewed the p11 expression to HPA and SAM axes limits
by analyzing p11 deficiencies in mice. The mice were tested using behavioural, endocrine, and
physiological readouts and were shown to have a higher heart rate and more anxiety with p11
definciencies (Sousa et al., 2020). In conclusion, p11 affects the initial release of cortisol (stress
hormone) in mice through modulation of specific neurons in the in the nerve centre part of the
brain (Sousa et al., 2020). As well, p11 seems to manage more than one pathway beginning in
the brainstem as it influences the arrival of two different stress hormones, adrenaline and
noradrenaline (Sousa et al., 2020). As per Sousa et al. (2020), the protein p11 directs the HPA
axes through adjustment of cell activity and was found to change the sensitivity of the heart
through 5-HT4 receptors. Most importantly, p11 shortage was found to slow the responsiveness
to antidepressants (Sousa et al., 2020).
The need for the study done by Karolinska Institutet is undeniable. According to Lowe
(2018), Graduate students from all over the world face ongoing amounts of stress and anxiety
and not surprisingly, the rate of students experiencing anxiety goes up each year. Graduate
students are more prone to experiencing depression and anxiety compared to other people
(Evans et al., 2018). Not known to many people, stress is a major contributor to physical
conditions. For example, the effects of stress on bone growth in which impaired bone growth,
specifically the growth plate, is observed in children that undergo stress (Sävendah, 2012).
Furthermore, the study relating to the effects of acute and chronic stress on Diabetes control
(not the cause of Diabetes). Stress can make hormonal changes that can influence glucose
homeostasis in both ordinary individuals and individuals with diabetes and can adversely affect
blood glucose concentrations in patients with type 1 and 2 diabetes (Marcovecchio & Chiarelli,
2012).
