Cognitive functions as mediators between emotion regulation, anxiety and depression in psoriasis

Arezoo Moradi Tavalaei1, Kiana Rahmati2, Mahdi Razmara3

1Department of Psychology, Imam Reza International University, Mashhad, Iran, 2Imam Reza Hospital, Mashhad University of Medical Sciences, Mashhad, Iran, 3Department of Dermatology, Imam Reza Hospital, Mashhad University of Medical Sciences, Mashhad, Iran

Corresponding author: Mahdi Razmara, MD, E-mail: dabir.jadbums@gmail.com
How to cite this article: Moradi Tavalaei A, Rahmati K, Razmara M. Cognitive functions as mediators between emotion regulation, anxiety and depression in psoriasis. Our Dermatol Online. 2026;17(4):448-456.
Submission: 10.06.2026; Acceptance: 19.08.2026
DOI: 10.7241/ourd.20264.3

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© Our Dermatology Online 2026. No commercial re-use. See rights and permissions. Published by Our Dermatology Online.

ABSTRACT

Background: Psoriasis patients frequently experience depression and anxiety, yet the mechanisms underlying this relationship remain unclear. Cognitive dysfunction has been proposed as a potential contributor linking emotional regulation deficits with psychological distress in psoriasis.

Material and Methods: This study aimed to examine whether basic cognitive functions mediate the relationship between emotion regulation and psychological distress—including depression and anxiety—in individuals with psoriasis. In this cross-sectional study, 90 psoriasis patients completed the Emotion Regulation Questionnaire (ERQ), the Montreal Cognitive Assessment (MoCA), and the Depression, Anxiety, and Stress Scale (DASS-21). Disease severity was assessed using the Psoriasis Area and Severity Index (PASI). Data was analyzed using Partial Least Squares Structural Equation Modeling (PLS-SEM).

Results: Cognitive functions significantly mediated the relationship between emotion regulation and both depression (β = -0.20, p < 0.01) and anxiety (β = -0.18, p < 0.01). Higher PASI scores correlated with poorer cognitive function (r = -0.44, p < 0.001), and with higher levels of depression (r = 0.61, p < 0.001) and anxiety (r = 0.64, p < 0.001).

Conclusion: Cognitive impairment may underlie psychological distress in psoriasis. These findings support the hypothesis that neuroinflammatory mechanisms may simultaneously impair cognitive function and emotion regulation. Integrating cognitive screening and interventions into psychodermatological care could improve mental health outcomes in psoriasis patients.

Key words: Anxiety, Cognition, Depression, Emotion Regulation, Psoriasis

INTRODUCTION

Psoriasis is a chronic inflammatory skin disease affecting both men and women equally. Psoriasis affects approximately 2–3% of the global population, with rising incidence linked to urbanization and environmental triggers [1]. Genetic and environmental factors contribute to its etiology, with triggers including medications, infections, psychological stress and trauma [2]. Given the role of psychological factors in psoriasis onset and progression, it is classified as a psychosomatic disorder, as recognized in The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) [3]. These disorders manifest physically but stem from emotional causes, affecting autonomic nervous system function and endocrine activity [4].

Psoriasis can affect all body parts, including the face and genital areas, making it a significant source of distress. Visible skin lesions can provoke negative social reactions, leading to emotional distress, helplessness and decreased quality of life [5–7]. Psychological comorbidities, including depression and anxiety, are prevalent among psoriasis patients, often worsening disease outcomes and treatment response [8–10].

Given the strong association between stress and psoriasis, emotion regulation plays a crucial role in managing disease impact [11]. Emotion regulation involves strategies for modifying emotional experiences, including cognitive reappraisal, rumination, avoidance and suppression [12,13]. Emotion regulation allows individuals to harness beneficial emotions while mitigating harmful ones [14]. Research has shown that psoriasis patients struggle with emotion regulation, exhibiting emotional rigidity and social withdrawal, which negatively impact disease severity and psychological well-being [15,16]. Patients with poor emotion regulation tend to experience more severe psoriasis symptoms and psychological distress [17]. Pro-inflammatory cytokines (e.g., IL-6, TNF-α) in psoriasis may directly impair prefrontal cortex function, disrupting both cognitive control and emotion regulation [18–21].

Executive functions and cognitive abilities play a key role in emotion regulation. Studies indicate a strong relationship between cognitive deficits and impaired emotion regulation. Patients with cognitive impairments show greater difficulties in managing emotions, which may exacerbate psoriasis severity [16,17,22]. Recent research suggests that psoriasis patients may experience cognitive deficits, particularly in executive function, attention, and memory. For instance, a study reported mild cognitive impairment (MCI) in individuals with chronic plaque psoriasis, a condition that, while not yet disruptive to daily life, increases the risk of neurodegenerative disorders like Alzheimer’s disease [23]. Similarly, a cross-sectional study using the Montreal Cognitive Assessment (MoCA) found deficits in visuospatial abilities and executive function among psoriasis patients [24]. Given the role of psychological stressors in exacerbating psoriasis, cognitive impairments may not only affect mental health but also contribute to disease progression by influencing emotion regulation.

Despite growing evidence of cognitive dysfunction in psoriasis, the interplay between cognition, emotion regulation and psychological distress remains poorly understood. While prior research has focused on direct psychological links, no study has examined cognitive functions as a mediator between emotion regulation and mental health in psoriasis-a gap addressed here using advanced SEM methods. Additionally, few studies have explored how disease severity may moderate these interactions. Considering the psychosomatic nature of psoriasis and the limited psychological research in this domain, there is a critical gap in understanding how cognitive and emotional processes interact to shape patients’ mental health outcomes. The present study investigates the mediating role of basic cognitive functions in the relationship between emotion regulation and depression/anxiety in psoriasis patients, while also assessing the impact of disease severity, an aspect rarely considered in prior research.

MATERIAL AND METHODS

Study Design

This study employed a cross-sectional clinical study design to examine the mediating role of basic cognitive functions in the relationship between emotion regulation and depression/anxiety in psoriasis patients. The study was conducted at the skin clinic of Imam Reza Hospital in Mashhad in 2018-2019.

Participants

A total of 90 participants diagnosed with psoriasis were recruited using a convenience sampling method. Participants were included if they had a clinical diagnosis of psoriasis confirmed by a dermatologist, were between 18 and 50 years old including both male and female participants, had at least a high school diploma and were right-handed. Participants were excluded if they had a history of major neurological or psychiatric disorders other than depression or anxiety, if they were using psychiatric medications, if they had other acute physical illnesses, if they had intellectual disability or other cognitive impairments.

Procedure and Materials

Participants were recruited from dermatology clinics. After obtaining written informed consent, they completed a set of psychological and cognitive assessments in a single session lasting approximately 60 minutes. The assessments included:

Emotion Regulation Questionnaire (ERQ)

A questionnaire developed by Gross and John (2003) was used to measure emotion regulation [25]. It consists of a 10-item checklist divided into two subscales, capturing cognitive reappraisal and expressive suppression as two of the most common emotion regulation strategies. Reappraisal involves thinking differently about a possible stressor event to manage the emotional response better, whereas suppression refers to a diminished or inhibited response to the same event. We asked participants to rate their usual ways of regulating their emotions on a 7-point Likert scale (1 = totally disagree to 7 = totally agree). Higher scores indicate a higher tendency to adopt a particular strategy. Global value of emotion regulation is determined by the total score on ERQ. The internal consistency for expressive suppression and cognitive reappraisal was 0.73 and 0.79, respectively. The original version of the ERQ demonstrated strong internal consistency, validity, and test-retest reliability [25]. The Persian adaptation also showed acceptable psychometric properties, with internal consistency scores of 0.87 for reappraisal and 0.85 for suppression and test-retest reliability coefficients of 0.71 and 0.68, respectively [26]. In the present study, both ERQ subscales showed good internal consistency, with Cronbach’s alpha value of 0.83 for reappraisal and 0.79 for suppression.

Montreal Cognitive Assessment (MoCA)

MoCA is a psychometric test developed by Nasreddine et al. for assessing mild cognitive impairment. It has been demonstrated that MoCA has a high sensitivity for detecting MCI (90%) and Alzheimer’s disease (100%) [27]. A score of 24 has been established as the cutoff point for the assessment. This test is one page long and can be completed in less than 15 minutes. There are eight cognitive domains evaluated in the test, including short-term memory (delayed recall), visuospatial skills (cube drawing and clock drawing), executive function (making trails with numbers and letters, verbal fluency and abstraction), attention, concentration, working memory (digit span, subtraction and serial counting), language (naming and sentence repetition) and orientation. The scoring system is as follows: a score of 26 or higher is considered normal, while a score below 26 indicates Alzheimer’s disease or MCI. A point is added to the total score for individuals with less than 12 years of education. In a study conducted in Iran to examine the psychometric properties of the Montreal Cognitive Assessment (MoCA) scale in Parkinson’s patients, the results indicated a Cronbach’s alpha reliability coefficient of 0.77 [28]. In this study, MoCA showed good internal consistency. According to Cronbach’s alpha, this test had a 92% reliability and an 83% internal consistency.

Depression, Anxiety, and Stress Scale (DASS-21)

This scale measures psychological constructs of depression, anxiety, and stress. An original version of the DASS had 42 items, which has since been shortened to 21 items (DASS-21) [29]. There are seven items on each subscale of DASS-21 and the final score is calculated by adding the scores. The items are scored on a 0 to 3 scale. As DASS-21 is a shortened version of the original scale, the total score for each subscale must be doubled before comparing it to the severity classification Table 1. A study conducted in Iran evaluated the internal consistency reliability and construct validity of the Persian version of the DASS-21. Findings from that study indicated strong internal consistency, with Cronbach’s alpha values of 0.88 for both the depression and anxiety subscales, 0.89 for the stress subscale, and an overall reliability coefficient of 0.93 [30]. In this study, the internal consistency coefficients for depression, anxiety, and stress were 0.93, 0.90, and 0.92, respectively, and test-retest reliability over a three-week period were 0.84, 0.89, and 0.90. In addition, an intraclass correlation of 0.78, 0.87, and 0.80 was found between two test administrations, indicating adequate reliability.

Table 1: DASS-21 severity classification.

Psoriasis Area and Severity Index (PASI)

It is a tool used to assess the severity and progression of psoriasis. Representative psoriasis-affected areas are selected for different body regions, including the head and neck, upper limbs, trunk, and lower limbs. The severity of erythema (redness), thickness and scaling of psoriasis is rated as none (0), mild (1), moderate (2) severe (3) or very severe (4). The intensity scores for each body region are summed as A1, A2, A3 and A4. Each subset is then multiplied by the proportion of the affected body area, calculated as follows:

A1 × 0.1 = B1

A2 × 0.2 = B2

A3 × 0.3 = B3

A4 × 0.4 = B4

Psoriasis is assessed across four body regions, with the affected area categorized as follows: 0% (0), 1–9% (1), 10–29% (2), 30–49% (3), 50–69% (4), 70–89% (5) or 90–100% (6). The final score is calculated by multiplying each regional severity score by the respective affected body area:

B1 × (0–6) = C1

B2 × (0–6) = C2

B3 × (0–6) = C3

B4 × (0–6) = C4

The total PASI score is reported as a numerical value. A score below 10 indicates mild psoriasis, whereas a score above 10 suggests moderate to severe psoriasis [1].

Cognitive assessments and PASI score were administered by trained researchers while other questionnaires were self-reported.

Ethical Considerations

This study was approved by the ethics committee of Mashhad University of Medical Sciences. Written informed consent was obtained from all participants before participation.

Statistical Analysis

Data analysis proceeded in two stages: (1) Preliminary analyses (SPSS v26) included descriptive statistics and normality checks (Shapiro-Wilk), and (2) Primary analysis used Partial Least Squares SEM (Smart PLS 3.3.9) with 5000 bootstrap samples to test the hypothesized model. PLS-SEM was selected for its robustness to non-normal data and small samples, evaluating both measurement model (reliability/validity) and structural relationships (path coefficients with |t| > 1.96, p <.05). Mediation was confirmed via Sobel tests and R² effect sizes.

RESULTS

Study Sample and Demographic Data

The study included 90 consecutively recruited psoriasis patients (mean age = 32.4 ± 8.8 years; range: 19–49) from a tertiary dermatology center. The sample comprised slightly more females (52.2%, n=47) than males (47.8%, n=43), with the majority (77.8%) aged below 40 years. Demographic characteristics revealed a predominantly married (64.4%), educated population (39.9% held bachelor’s degrees or higher) and diverse occupational status (32.2% self-employed, 25.6% employees). Complete demographic data is presented in Table 2.

Table 2: Patients’ demographic characteristics.

Descriptive Statistics of Study Variables

Among the participants (N=90), the mean anxiety score was 10.87 (SD = 6.19), while the average depression score was 7.08 (SD = 3.82). The mean score for cognitive emotion regulation was 30.84 (SD = 7.79), and for basic cognitive functions, it was 24.14 (SD = 3.29). The average psoriasis severity score was 17.98 (SD = 12.22), ranging from 3.4 to 51.00. For detailed information on the range and maximum possible scores for each variable, refer to Table 3.

Table 3: Descriptive findings of study scales.

Our Spearman correlation analysis (selected due to non-normal data distribution) revealed significant associations between psoriasis severity and key study variables (Table 4). The most robust findings showed:

  • Inverse relationships: Psoriasis severity demonstrated moderate negative correlations with both cognitive function (r = -0.44, p<0.001) and emotion regulation capacity (r = -0.31, p<0.001).
  • Positive relationships: Strong positive correlations emerged between disease severity and depression (r = 0.61, p<0.001). Similarly strong association with anxiety (r = 0.64, p<0.001)

Table 4: Spearman correlation matrix.

Notably, cognitive function showed particularly strong inverse relationships with both depression (r = -0.71) and anxiety (r = -0.69), suggesting its potential mediating role in the psoriasis-psychopathology pathway. These correlation patterns provide empirical support for our conceptual model integrating biological and psychological disease dimensions.

Analytical Approach

We employed Partial Least Squares Structural Equation Modeling (PLS-SEM) to examine the hypothesized relationships among latent constructions. The analysis proceeded in two phases:

  1. Measurement Model Evaluation:

All latent constructions demonstrated satisfactory reliability and validity:

  • Factor loadings > 0.7 (Table 4)
  • Composite reliability (CR) > 0.8
  • Average variance extracted (AVE) > 0.5.
  1. Structural Model Assessment:

The model exhibited a good fit:

  • SRMR = 0.042 (≤ 0.08 threshold)
  • NFI = 0.93 (≥ 0.90 threshold)

Path coefficients were evaluated using bootstrap t-tests (5000 samples), with |t| > 1.96 and p < 0.05 indicating significance (Figs 1–2).

Figure 1: Proposed research model in the case of estimating standardized factors loading coefficients.
Figure 2: Proposed research model in the case of significant coefficients.

Analysis

The partial least squares structural equation modeling (PLS-SEM) analysis demonstrated significant pathway coefficients in our proposed model (all p < 0.001):

  1. Direct Effects:
  • Emotion regulation had a strong negative effect on anxiety (β = −0.609, t = 11.295) and depression (β = −0.763, t = 22.374), indicating that poorer emotion regulation predicts higher psychological distress.
  • Conversely, emotion regulation positively influenced core cognitive functions (β = 0.575, t = 9.307), suggesting better emotional control is associated with enhanced cognition.
  • Cognitive functions, in turn, negatively impacted both anxiety (β = −0.533, t = 4.247) and depression (β = −0.357, t = 4.537).
  1. Mediation Effects:
  • Cognitive functions partially mediated the link between emotion regulation and anxiety (indirect effect: β = −0.306, t = 3.526), accounting for 33.5% of the total effect.
  • Similarly, mediation was observed for depression (indirect effect: β = −0.205, t = 3.885), explaining 26.8% of the total effect. Further details are presented in Table 5.
  1. Model Fit:

All paths exceeded the critical t-value threshold of 1.96 (p < 0.001), with satisfactory model fit indices (SRMR < 0.08; NFI > 0.90), supporting the robustness of our hypothesized relationships.

Table 5: Direct and indirect effects of emotion regulation on anxiety and depression.

Mediation Analysis Results

The statistical significance of cognitive functions as a mediator was confirmed through complementary analyses:

1. Sobel Test Results:

  • For the emotion regulation → cognition → depression pathway:
  • Sobel z = -4.09, p <.001 (two-tailed)
  • For the emotion regulation → cognition → anxiety pathway:

Sobel z = -3.72, p <.001 (two-tailed)

These results robustly support the mediating role of cognitive functions (p-values <.001 for both pathways).

2. PLS-SEM Path Analysis:

The structural model revealed:

  • Emotion regulation significantly predicted cognitive functions (β = 0.58, t = 8.41, p <.001), accounting for 33% of variance (R² = 0.33)
  • Significant negative direct effects were found:
  • Emotion regulation → anxiety: β = -0.56, t = 2.84, p <.01
  • Emotion regulation → depression: β = -0.30, t = 8.35, p <.001
  • Cognitive functions showed significant negative paths to both anxiety (β = -0.53) and depression (β = -0.36).

Key Interpretation

The convergence between Sobel test and PLS-SEM results provides strong evidence that cognitive functions serve as a partial mediator in the observed relationships, explaining approximately 26-34% of the total effects (based on effect size calculations).

DISCUSSION

This study aimed to investigate the mediating role of basic cognitive functions in the relationship between emotion regulation and psychological outcomes such as depression and anxiety in patients with psoriasis. The findings revealed that basic cognitive functions significantly mediate the association between emotion regulation and both depression and anxiety. To our knowledge, this is the first study to examine this specific mediation model in patients with psoriasis, as no directly comparable studies were identified in literature.

Beyond psychological symptoms, our results also shed light on the connection between emotion regulation ability and disease severity in psoriasis. In line with previous findings [16,17,31], we observed a significant negative correlation between emotion regulation and psoriasis severity, reinforcing the notion that greater difficulties in regulating emotions may be associated with increased clinical burden [32]. This suggests that impaired emotion regulation could not only affect psychological well-being but also exacerbate disease outcomes in psoriasis [33].

Our data also revealed a significant negative correlation between basic cognitive functioning and disease severity. While only one previous study has explored link-reporting deficits in visuospatial and executive functions without finding a direct association with disease characteristics, our findings diverged, likely due to methodological advantages such as a broader range of severity and better demographic matching in our sample [24]. These results suggest that cognitive impairment may be more intricately tied to the clinical presentation of psoriasis than previously assumed.

Furthermore, consistent with past research on the emotional consequences of disease burden [34], we observed strong positive correlations between disease severity and both depression and anxiety. This reinforces the interpretation that patients with higher disease burden are at greater risk of emotional distress [35]. Considering these patterns, it becomes evident that individuals with poorer emotion regulation and cognitive functioning also tend to exhibit higher disease severity [16,17,24,31], which in turn predicts more severe depressive and anxiety symptoms [36].

This interconnected pattern of relationships supports the hypothesis that both emotion regulation and cognitive ability are indirectly linked to psychological symptoms. Prior literature, along with our current findings, highlights a plausible pathway where cognitive function not only reflects underlying disease mechanisms but also plays a key role in the emotional adjustment of patients with psoriasis [37]. Additionally, our data aligns with previous research showing a direct link between emotion regulation and basic cognitive ability, strengthening the overall model [38].

From a neurophysiological perspective, these findings can be interpreted within the framework of systemic inflammation and its impact on brain function. Psoriasis is increasingly understood as a systemic inflammatory condition characterized by elevated pro-inflammatory cytokines such as IL-6 and TNF-α [19], which have been consistently associated with cognitive decline [39]. Chronic inflammation has been shown to impair attention, processing speed, memory and cognitive flexibility [40–42] domains closely tied to emotion regulation [43,44].

Disruptions in these cognitive domains, particularly those involving the prefrontal cortex and anterior cingulate cortex, have been implicated in the impaired regulation of emotional responses, especially under conditions of stress [45,46]. These brain regions are crucial for executive functioning and are frequently dysregulated in mood disorders [47]. Taking together, existing neurobiological and psychological research supports an integrated model in which systemic inflammation contributes to cognitive impairments [48], which subsequently weakens emotion regulation [38] and heightens vulnerability to depression and anxiety [49].

Ultimately, our findings suggest that basic cognitive functions serve as a crucial mediator in the link between emotion regulation and psychological symptoms in individuals with psoriasis. This highlights the need for a more comprehensive clinical approach-one that considers cognitive and emotional factors alongside dermatological treatment in managing this complex disease.

CONCLUSION

This study provides novel evidence that cognitive dysfunction serves as a significant mediator between emotion regulation difficulties and psychological distress in psoriasis patients, explaining 26-34% of these relationships. The strong associations between disease severity, cognitive impairment, and mood symptoms suggest that psoriasis-related systemic inflammation may concurrently disrupt both cognitive and emotional processing pathways. These findings advocate integrated psychodermatological care incorporating cognitive screening and targeted interventions to address the mind-skin connection, potentially improving both mental health outcomes and disease management. Future research should explore whether modulating these cognitive-emotional factors can influence psoriasis progression, offering new avenues for holistic treatment approaches.

LIMITATIONS AND FUTURE RESEARCH

While this study provides valuable insights, several limitations should be considered:

  1. The modest sample size (N=90) from a single clinic may limit generalizability; future multi-center studies with larger, more diverse cohorts are needed to validate these findings.
  2. Cross-sectional design prevents causal inferences; longitudinal studies tracking cognitive-emotional changes before/after treatment would clarify temporal relationships.
  3. Reliance on screening tools (MoCA) rather than comprehensive neuropsychological assessments may overlook subtle cognitive deficits; future work should incorporate detailed cognitive batteries.
  4. Unexamined medical variables (e.g., treatment duration, comorbidities) and psychological factors (e.g., trauma history, personality) may influence outcomes; these should be systematically controlled in subsequent research.

Statement of Human and Animal Rights

All the procedures followed were in accordance with the ethical standards of the committee responsible on human experimentation (institutional and national) and with the 2008 revision of the Declaration of Helsinki of 1975.

Statement of Informed Consent

Informed consent for participation in this study was obtained from all patients.

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