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Ann. psychophysiol. 
ISSN 2412-3188 (Online) | 2410-1354 (Print) 

 
 
Original Article                                                                                  

Assessment of Cortisol, Brain-Derived 
Neurotropic factor, C - reactive protein, 
Interleukin-6 levels and cognitive decline 
after trauma exposure 
Shamoon Noushad1,2 , Ujala Sajid3, Sadaf Ahmed2,3  & Basit Ansari1  

1Department of Health & Physical Education, University of Karachi, Karachi-Pakistan. 

2Psychophysiology Research Lab, MAHQ Biological Research Centre, University of Karachi, 

Karachi-Pakistan. 

3Department of Physiology, University of Karachi, Karachi-Pakistan. 

Abstract 
Background: Studies have found that multiple neurobiological mechanisms are 
underlying the cause of Posttraumatic stress that influence the nervous and 
immune system leading to neurodegenerative and psychiatric comorbidities. The 
present study aims to assess and evaluate the serum Cortisol, C - reactive protein 
(CRP), Interleukin-6 (IL-6), Brain-Derived Neurotropic Factor (BDNF) levels and 
cognitive decline among subjects with trauma exposure and to determine the 
relationship between the above-specified stress biomarkers. 
Methodology: Two groups with trauma exposure (including natural disaster, any 
accident, physical and/or verbal violence, or any stressful condition) in the last 
twelve months were recruited. Groups were majorly divided based on TSC-40 
(Trauma Symptom Checklist - 40) scores. Subjects with a TSC score > 40 were kept 
in the traumatized group, while those with TSC score < 40 were included in the 
control group. A total of 188 subjects above the age of 18 were recruited following 
inclusion criteria, cognition was measured using the Six-Item Cognitive 
Impairment Test (6-CIT), and serum samples were obtained for cortisol, CRP, 
BDNF, and IL-6 levels. 
Results: There was a significant difference in the serum BDNF (p<0.001) level 
among the traumatized subjects, i.e. 15.68 ± 3.55 ng/dl as compared to controls 
26.65 ± 2.47 ng/dl; no significant difference was found in CRP levels (ns) in both 
groups with a slight increase among the traumatized subjects as compared to the 
controls, i.e. 4.29 ± 1.50 mg/dl vs. 3.42 ± 1.11 mg/dl. As indicated by the 6-CIT 
score, the cognitive decline was more pronounced among the traumatized 
subjects, i.e. 8.54 ± 2.13 compared to the control group 5.0 ± 1.81, with a significant 
positive difference (p<0.001). 
Conclusion: The finding suggests that traumatic stress is associated with 
Cognitive decline, BDNF and cortisol, whereas a non-significant association was 
found with IL-6 and CRP levels. 

Keywords 
Traumatic Stress, Cognitive Decline, Brain-Derived Neurotrophic Factor, C - 

reactive protein, Interleukin-6, Cortisol. 

Citation: Noushad S, Sajid U, Ahmed S. 
& Ansari B. Assessment of Cortisol, 
Brain-Derived Neurotropic factor, C - 
reactive protein and Interleukin-6 levels 
as well as cognitive decline after trauma 
exposure. APP.2021; 8(1):6-14 
 
Corresponding Author Email: 
ujalasajid97@gmail.com 
 
DOI: 10.29052/2412-3188.v8.i1.2021.6-14 
 
Received 01/01/2021 
 
Accepted 07/04/2021 
 
Published 01/06/2021 
 
Copyright © The Author(s). 2021 This  
 is an open-access article distributed 
under the terms of the Creative 
Commons Attribution 4.0 International 
License, which permits unrestricted use, 
distribution, and reproduction in any 
medium, provided the original author 
and source are credited.  
 

 

Funding: The author(s) received no 
specific funding for this work. 

Conflicts of Interests: The authors 
have declared that no competing 
interests exist. 
 

https://doi.org/10.29052/2412-3188.v8.i1.2020.
https://orcid.org/0000-0002-8078-4524
https://orcid.org/0000-0002-9635-0202
https://orcid.org/0000-0003-3919-2516
http://creativecommons.org/licenses/by/4.0/)
http://creativecommons.org/licenses/by/4.0/)
http://creativecommons.org/licenses/by/4.0/)


 
 
 

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Introduction  
Traumatic events and associated stress have 
been known to trigger several physical or 
mental health disabilities, including fatigue, 
sleep disturbances, anxiety disorder, 
depression etc. A debate has continued for 
decades until several studies have proposed 
a significant link between traumatic stress 
and its psychological impact on individuals' 
health and well-being1, 2. The drastic or life-
threatening events, including accidents, 
natural disasters, physical and/or verbal 
violence, or any other stressful condition that 
is a source of trauma and alters the body's 
homeostasis, leads to traumatic stress3. 
Individuals with mental health problems 
such as Post-Traumatic Stress Disorder 
(PTSD) and major depressive disorder 
(MDD) or even psychiatric problems had 
mostly experienced certain traumatic 
incidences like early childhood trauma, 
sexual abuse, verbal abuse, and physical 
violation2,4-6. Moreover, the traumatic 
subjects tend to have a reduced ability to 
cope with fear and usually feel helpless most 
of the time7. This coping disability generally 
leads to PTSD that is considered a 
heterogeneous condition6 and characterized 
by successive traumatic reminders, 
avoidance of cue related to trauma, negative 
cognition, etc3, 8. 
 
In the current era, traumatic events are very 
common in one's life, leading to severe 
psychotic distress and neuronal impairment; 
it should be assisted by clinicians, 
psychologists or psychotherapists, either by 
interviewing the traumatized individual any 
formal psychometric testing or any 
assessment tool9. Early assessment and 
effective management has shown positive 
growth among the traumatized individuals 
depending upon the type and number of 
experiences of the traumatic event10. Normal 
brain development needs to be reviewed at 
different life stages to understand how 

traumatic stress initiates5. From childhood to 
later in life, the human brain undergoes 
several changes, be it structural or 
functional. It is essential to be well aware of 
the normal developmental changes to 
differentiate them based on the pathologies5. 
It is important to understand the changes in 
individual behaviour, both mentally and 
socially, caused by any stressful situation or 
trauma experiencing. Previous evidence 
from studies has associated childhood 
victimization or trauma, decades after 
exposure, with an elevation of inflammatory 
biomarkers measured8.  
 
Evidence suggests that the subjects who had 
suffered from childhood victimization or 
trauma have elevated levels of inflammatory 
biomarkers, including IL-6 and CRP, while 
relatively low levels of BDNF8,10. The 
involvement of neurobiological 
inflammatory markers in the pathogenesis of 
trauma is quite obvious. CRP is the most 
validated and widely studied biomarkers of 
the peripheral inflammation associated with 
trauma9, and elevated CRP levels indicate 
the increased risk of degenerative 
disorders11. Similarly, BDNF is one of the 
most extensively researched neurotrophic 
factors with the most established evidence of 
influencing synaptic plasticity and has a 
significant role in cellular proliferation and 
brain pathologies12,13. The down regulation 
of BDNF in association with traumatic 
history results in long-term changes in the 
neurobiology of the brain, suggesting BDNF 
as an essential biomarker of pathological 
conditions14.  
 
In the behavioural literature, both of the 
molecules that is IL-6 and CRP regarded as 
inflammatory biomarkers and used mostly 
in assessing the presence and severity of 
low-grade inflammation15-17. Chronic stress 
leads to various disease states through the 
activation of two major systems i.e. HPA –



 
 
 

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axis and the other is the sympathetic nervous 
system (SNS) axis, usually by the up-
regulation of glucocorticoids (cortisol in 
humans) and catecholamines (epinephrine 
and norepinephrine)18. These two secreted 
molecules then perform their function by 
acting through their separate receptor 
mechanism on different cell types, including 
the immune cells and nerve cells18,16. Besides, 
it is suggested that chronic stress usually 
inhibits the secretion of proinflammatory 
cytokines that usually mediate cellular 
immunity. On the other hand, the stress can 
activate the anti-inflammatory cytokine that 
mediates humoral immunity. Based on this 
general hypothesis was led that chronic 
stress particularly leads towards the disease 
state through immunosuppression. 
 
However, there is still a gap in 
understanding the overall association of 
HPA axis activation that leads to alteration 
in the serum BDNF, IL-6, cortisol and CRP 
levels under pathological conditions. The 
present study aimed to assess and compare 
serum cortisol, CRP, IL-6, and BDNF levels 
among subjects with trauma exposure and to 
determine the relationship between the 
above-specified stress biomarkers. The 
outcome of this study suggests a significant 
association between severity of trauma and 
decrease level of BDNF, along with slight 
elevation in the serum cortisol, CRP and IL-
6, highlighting the possible involvement of 
BDNF, CRP and IL-6 in the development of 
post-traumatic stress.  
 

Methodology 
This cross-sectional study was conducted 
from September to December 2019. Two 
groups with trauma exposure (including 
natural disaster, any accident, physical 
and/or verbal violence, or any stressful 
condition) in the last twelve months were 
recruited. Groups were majorly divided 
based on TSC-40 scores. Subjects with a TSC 

score > 40 were kept in a traumatized group, 
while those with < 40 scores were included 
in the control group. 
 
Subjects were recruited from the following 
three sites, i.e. University of Karachi, 
Markaz-e-Umeed and Kohi Goth Hospital. A 
total of 188 subjects above 18 years of age 
were recruited, with no evidence of any 
metastatic disease, were enrolled in the 
study. According to DSM-V, subjects having 
any codified psychiatric disorder, those on 
psychopharmacological treatment during 
the last three years and those who had gone 
through any structural, psychological 
intervention for at least six months during 
the last three years were kept under 
exclusion criteria. Pakistan medical 
association committee on ethics approved all 
recruitment and assessment procedures. All 
subjects included provided written informed 
consent after receiving a complete 
description of the study. 
 
For the investigation of traumatic symptoms, 
TSC-40 was used19. TSC-40 is a self-reported 
40-item inquiry form based on a 4-point 
Likert scale. It evaluates symptomatology in 
adults associated with childhood or adult 
traumatic experiences and measures aspects 
of posttraumatic stress and other symptom 
clusters found in some traumatized 
individuals. TSC-40 consisting of six 
subscales: Anxiety, Depression, 
Dissociation, Sexual Abuse Trauma Index 
(SATI), Sexual problems and sleep 
disturbances; it requires approximately 10-
15 minutes to complete. Cognition was 
measured using the 6-CIT18. This short 2-3-
minute test contains items on orientation, 
memory and concentration. Scoring ranges 
from 0-28, with higher scores indicating 
more cognitive impairment. Patients with a 
6-CIT score of 10 points or lower were 
considered normal cognition; those with 6-
CIT score ≥ 11 were categorized as cognitive 



 
 
 

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impairment20. Venous blood was collected 
For estimation of CRP, Cortisol, IL-6 and 
BDNF into sampling tubes in the morning, 
the concentration of CRP (mg/dl), BDNF 
(ng/dl), Cortisol (mcg/dl), IL-6 (pg/ml) was 
measured using enzyme-linked 
immunosorbent assay.  
 
All the continuous variables like age, 
Cortisol, CRP, BDNF, and TSC-40 score were 
expressed as mean and standard deviation. 
In contrast, the categorical variables, 
including gender, ethnicity, occupation and 
religious preference, etc., were given 
frequency and percentages.  
 

Chi-square test and One-way Analysis of 
Variance (ANOVA) were used for 
comparison between the groups, and p<0.05 
was considered statistically significant. Data 
were analyzed using SPSS Version 22.0. 
 

Results 
Out of 188 subjects, there were 88 

traumatized and 100 controls. The majority 

were females, i.e. 75%, and only 25% were 

males, with a mean age of 29 ± 7.8 years. 

Most of the subjects belonged to different 

ethnicity, had different occupational 

statuses, religious preferences and political 

views, as shown in (Table 1).  

 

Table 1: Demographic characteristics of the subjects enrolled in the study.  

Baseline Characteristics  n(%) 

Gender Male 47(25) 

Female 141(75) 

Ethnicity Sindhi 24(12.76) 

Balochi 23(12.23) 

Punjabi 18 (9.57) 

Pathan 21(11.17) 

Muhajir 80(42.55) 

Others 15(7.97) 

Prefer not to respond 7(3.19) 

Occupation Student (not working) 133(70.74) 

Student (part-time job/business) 13(6.91) 

Student (full-time job or business) 14(7.44) 

Business 11(5.85) 

Salaried Person 17(9.04) 

Religious preference Agnostic 2(1.06) 

Religious 165(87.76) 

Not religious but spiritual 14(7.44) 

Others 7(3.72) 

Political View Conservative 30(15.95) 

Moderate 118(62.76) 

Liberal 40(21.27) 

*Values are given as Mean ± SD or n(%) 



 
 
 

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Individuals with trauma (TCS Score > 40) had significantly lower levels of BDNF, i.e. 15.68 ± 3.55 

ng/dl, and slightly higher levels of CRP 4.29 ± 1.50 mg/dl as compared to controls (Table 2). 

 

Table 2: Comparative assessment of traumatic symptom and biomarkers among the 

traumatized and control subjects 

Variable  Traumatized (Group) Controls (Group) p-value 

Mean ± SD 

TSC-40 Score 56.72±11.91 27.76±9.28 <0.001* 

6-CIT Score 8.54±2.13 5.0±1.81 <0.001* 

CRP (mg/dl) 4.29±1.50 3.42±1.11 ns 

BDNF (ng/dl) 15.68±3.55 26.65±2.47 <0.001* 

Cortisol (mcg/dl) 26.17±3.65 20.37±3.71 <0.001* 

IL-6 (pg/ml) 2.90±0.63 2.44±2.08 ns 
*p-value < 0.05 is considered significant; ns: non-significant  

*TSC-40-Traumatic Symptom Checklist; 6-CIT-Six Item Cognitive Impairment Test; CRP-C-reactive 

protein; BDNF-Brain Derived Neurotropic Factor; IL-6-Interleukin 6 

 

 
Figure 1: Comparison of subscales scores of TSC-40 among the control  

and traumatized groups of study 

 

Figure 1 shows the mean value of the subscales score of TSC-40 among the traumatized and 

control subjects. Depression was significantly very high in traumatized subjects (X̅=14.02) 

compared to the control subjects (X̅=7.25). In contrast, the anxiety level was significantly also very 

high in traumatized residents (X̅=13.85) as compared to the control subjects (X̅=6.35). Dissociation, 

SATI, and Sleep disturbance level were almost equal in traumatized subjects with a mean value 

of 11.11, 9.22 and 10.45. Among all the subscales scores, both traumatize subjects and control 

subjects scored the lowest in the Sexual problem subscale; traumatized subjects (X̅=3.76) and 

control subjects (X̅=1.02). 

 

 

 

 

 

11.1

13.85 14.02

9.22
10.45

3.76

5.96 6.35
7.25

4.96
5.69

1.02

Dissociation Anxiety Depression Sati Sleep  Disturbance Sexual Problem

Traumatized Control



 
 
 

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Discussion 
The present study aimed to investigate the 
role of biomarkers in post-traumatic stress, 
focusing on the serum concentration of 
cortisol, BDNF, IL-6 and CRP among the 
traumatized and control subjects. The 
subjects who were deemed traumatized as 
per the findings from TSC-40, with 
comparatively high depression and anxiety 
index, were compared to those who scored 
less and considered as controls (Figure 1).    
 
The BDNF and CRP level was measured to 
find the association of inflammation with the 
underlying posttraumatic stress mechanism. 
Rosen et al., 2017 have suggested that 
systemic inflammation is associated with 
stress pathology with a positive CRP 
association with posttraumatic stress 
severity21. Moreover, a meta-analysis of 
random effects suggested that individuals 
who had experienced any type of childhood 
trauma (sexual, physical or emotional) had 
elevated baseline peripheral CRP levels17. A 
follow-up study by Laurin and his 
colleagues suggested that psychological 
distress is associated with increased CRP 
concentration and inflammatory 
mechanisms reflecting processes that further 
contribute to cognitive decline in later life22. 
Similarly, in our study, the mean CRP level 
was elevated among the traumatized 
subjects compared to the controls, i.e. 4.29 ± 
1.50 mg/dl vs. 3.42 ± 1.11 mg/dl (Table 2). 
Although the association wasn't significant 
as per the evidence, there was a prominent 
variation in the mean CRP level among the 
two groups. 
 
We found significant down regulation in the 
serum BDNF concentration among the 
traumatic subjects 15.68 ± 3.55 ng/dl as 
compared to the controls 26.65 ± 2.47 ng/dl 
(p<0.05) (Table 2). A recent study confirmed 
that the serum BDNF level decline among 
individuals with a history of a traumatic 

event or those with mental health illnesses14; 
the study indicated a significant decline in 
the serum BDNF concentration among 
patients reporting childhood sexual abuse 
and depressive episodes21. Moreover, 
Angelucci et al., in their study, suggested the 
involvement of BDNF in the 
pathophysiology of PTSD23. The role of 
BDNF in enhancing learning and memory in 
the hippocampus is evident24, and the 
present study revealed a positive correlation 
in the down-regulation of BDNF (Table 2).  
 
Our results show the positive correlation of 
cortisol with the TSC-40 score. The positive 
correlation shows that if the TSC-40 score 
increases, then the cortisol level also 
increases and vice versa. The increased score 
of TSC-40 indicates that people whose scores 
were above 40 have a high level of cortisol 
and the people whose TSC-40 score was 
below 40 have a low level of cortisol25. As a 
biomarker of stress, the cortisol is linked to 
the TSC-40 score, which determines the level 
of cortisol and trauma of an individual26. 
Thus, our finding also indicates higher the 
TSC-40 score, the higher the level of cortisol 
and this increase in cortisol level, the person 
can be identified in a chronic traumatic 
stress27. TSC-40 scores below 40 showed a 
decrease in levels of the IL-6, while the TSC-
40 scores above 40 showed an increase in IL-
6 levels though it was insignificant, as shown 
in table1that may indicate the initiation of 
low-grade inflammation28.   
 
Cognitive impairment is one of the core 
features of degenerative disorders, and 
studies showed a significantly high 
association between traumatic events, 
degeneration of brain cells and cognitive 
dysfunction29. The cognitive impairment 
among the traumatized subjects was 
significantly high compared to the control 
group, with a decreased level of BDNF. 
Studies have suggested that BDNF plays a 



 
 
 

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critical role in enhancing learning and 
memory in the hippocampus30. The results of 
6-CIT of a traumatized group show a 
positive correlation between the decreased 
level of BDNF levels with cognitive 
impairment pathology. There was a slight 
elevation in CRP and IL6 concentration in 
traumatized subjects compared to the 
control group, suggesting that higher CRP 
levels may be a marker of memory and 
learning impairment in traumatic subjects. 
Noble, J. M. et al., 2010, in a cross-sectional 
analysis, suggested that increased CRP level 
can be a marker of memory and an increased 
risk of cognitive decline31. Since the results 
show a very slight elevation in CRP levels of 
traumatized individuals, hence basis on the 
results, we cannot suggest an association 
between cognitive impairment and an 
increase in IL6 and CRP. 
  
These overall results indicate that some other 
undefined factors may be modifying the 
observed associations of traumatic events 
with degeneration of brain cells, related 
immune influences, and susceptibility to 
cause psychiatric conditions later in life by 
way of inflammatory processes32. Still, it is 
possible that changes in BDNF and cortisol 
while non-significance of IL6 and CRP can be 
assumed to certain specific characteristic 
symptoms of traumatic stress32,33. However, 
further exploration of the role of 
environmental interactions and immune 
mechanisms is still a challenge34. The 
limitations of the current study that hinder 
further insight include its focus on a cross-
sectional association based on one-time 
assessments of inflammatory markers, 
undervaluing the explicit inflammation 
markers' role in stress disorders and lack of 
longitudinal study design.  The symptomatic 
expositions and potential confounders 
interfering with the immune system should 
be monitored in longitudinal and case-
control settings to clarify these ambiguities.  

Conclusion 
The finding suggests that traumatic stress is 
associated with Cognitive decline, BDNF 
and cortisol, highlighting the possible 
involvement of these biomarkers in 
developing associated symptomatic 
neurobiological alterations. Whereas the 
changes in IL-6 and CRP were non-
significant in the association with traumatic 
scores. However, there is a possible role of 
the explicit inflammation markers, and 
related mechanisms that are needed to be 
explored by further large-scale descriptive 
studies or randomized controlled trials are 
required to elucidate the mechanism. 
 

Acknowledgment  
The authors are thankful to the participating 
institutes for the support and collaboration, 
and we also like to acknowledge the study 
participants for their kind cooperation. 
 

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