Background: Responses to stressful circumstances have psychological and physiological dimensions, and are related to anxiety symptoms and mental disorders such as depression. Nonetheless, the relationship between subclinical stress and anxiety symptoms is still elusive. Methods: To explore possible associations between stress and anxiety symptoms, patients with major depression (N = 77) and mentally healthy individuals of different age clusters and occupations (N = 412) were enrolled into the study. Stress was assessed with the new subclinical stress symptom questionnaire (SSQ-25). Anxiety was studied with the Beck Anxiety Inventory (BAI), mainly focusing on clinical anxiety, whilst anxiety as a personality trait was assessed with the trait aspect of the State Τrait Αnxiety Ιnventory Y (STAI Y). Statistical analyses included ANOVA, Scheffe test, linear regression models and a two-step cluster analysis using Log-Likelihood Distance measure and fixed number of two clusters. Results: Age, stress symptoms and BAI scores differed significantly between among groups (P < 0.001), whilst STAI Y scores did not. Stress levels were found to be related to clinical anxiety (P < 0.001), while neither group identity nor age exerted any influence on anxiety levels (P > 0.05). The two Step Cluster analysis classified 76 out of 77 participants with milder stress (subclinical) symptoms into the cluster with moderate anxiety, as indicated by BAI scores, and all individuals with more severe stress into the severe anxiety cluster. Conclusions: The observed associations between stress and anxiety shed light on the interrelations between even very mild (subclinical) stress and anxiety symptoms and may point to the potential of mild stress to serve as a target for early interventions aiming to prevent anxiety morbidity.

Alterations in the expression of human kallikrein-related peptidases (KLKs) have been described in patients with Alzheimer’s disease (AD). We elucidated the suitability of KLK6, KLK8 and KLK10 to distinguish AD from NC and explored associations with established AD biomarkers. KLK levels in cerebrospinal fluid (CSF), as determined by ELISA, were compared between 32 AD patients stratified to A/T/(N) system with evidence for amyloid pathology and of 23 normal controls with normal AD biomarkers. Associations between KLK levels and clinical severity, CSF and positron emission tomography (PET) based AD biomarkers were tested for. Levels of KLK6 and KLK10 were significantly increased in AD. KLK6 differed significantly between AD A+/T+/N+ and AD A+/T−/N+ or NC with an AUC of 0.922. CSF pTau and tTau levels were significantly associated with KLK6 in AD. KLK6 deserves further investigations as a potential biomarker of Tau pathology in AD.

Background: Detecting impaired naming capacity is valuable in diagnosing neurocognitive disorders (ND). A. clinical practice- oriented overview of naming tests validated in ND is not available yet. Here, features of naming tests with validated utility in ND which are open access or available for purchase are succinctly presented and compared. Methods: Searches were carried out across Pubmed, Medline and Google Scholar. Additional studies were identified by searching reference lists. Only peer-reviewed journal articles were eligible. A narrative- and tabullar synthesis was used to summarize different aspects of the naming assessment instruments used in patients with ND such as stimuli type, administration time, assessment parameters and accessibility. Based on computational word frequency calculations, the tests were compared in terms of the average frequency of their linguistic content. Results: Twelve naming tests, relying either on visual or auditory stimuli have been validated in ND. Their content and administration time vary between three and 60 items and one and 20 minutes, respectively. The average frequency of the words of each considered test was two or lower, pointing to low frequency of most items. In all but one test, scoring systems are exclusively based on correctly named items. Seven instruments are open access and four are available in more than one language. Conclusions: Gaining insights into naming tests’ characteristics may catalyze the wide incorporation of those with short administration time but high diagnostic accuracy into the diagnostic workup of ND at primary healthcare and of extensive, visual or auditory ones into the diagnostic endeavors of memory clinics, as well as of secondary and tertiary brain healthcare settings.

According to new diagnostic guidelines for Alzheimer’s disease (AD), biomarkers enable estimation of the individual likelihood of underlying AD pathophysiology and the associated risk of progression to AD dementia for patients with mild cognitive impairment (MCI). Nonetheless, how conflicting biomarker constellations affect the progression risk is still elusive. The present study explored the impact of different cerebrospinal fluid (CSF) biomarker constellations on the progression risk of MCI patients. A multicentre cohort of 469 patients with MCI and available CSF biomarker results and clinical follow-up data was considered. Biomarker values were categorized as positive for AD, negative or borderline. Progression risk differences between patients with different constellations of total Tau (t-Tau), phosphorylated Tau at threonine 181 (p-Tau) and amyloid-beta 1–42 (Aβ42) were studied. Group comparison analyses and Cox regression models were employed. Patients with all biomarkers positive for AD (N = 145) had the highest hazard for progression to dementia due to AD, whilst patients with no positive biomarkers (N = 111) had the lowest. The risk of patients with only abnormal p-Tau and/or t-Tau (N = 49) or with positive Aβ42 in combination with positive t-Tau or p-Tau (N = 119) is significantly lower than that of patients with all biomarkers positive. The risk of progression to dementia due to AD differs between patients with different CSF biomarker constellations.

Background: Recently, cognitive deficits occurring in rheumatic diseases have attracted scientific attention. Cognitive symptoms in patients with Rheumatoid Arthritis (RA) and Systemic Sclerosis (SSc) have not been thoroughly studied. This study aimed to assess cognitive function and its relationship with depressive symptoms in RA and SSc and compare it to mild neurocognitive disorder due to Alzheimer’s disease (MiND) and to individuals without cognitive impairment. Methods: Cognitive function and depressive symptoms were tapped with the Cognitive Telephone Screening Instrument plus (COGTEL+), the Serial Seven Test (SST), the Mini-Mental State Examination (MMSE) and the Geriatric Depression scale-15 (GDS), respectively. Statistical analyses included between groups-, correlation- and regression analyses. Demographic characteristics were considered in the regression models. Results: The study included 30 individuals with RA, 24 with SSc, 26 adults without cognitive impairment and 33 individuals with MiND. Lower performance in verbal short-term memory, concentration/attention, verbal fluency and MMSE in patients with RA compared to individuals without cognitive impairment was detected. Of note, performance on verbal fluency, concentration/attention, inductive reasoning and MMSE was lower in RA compared to MiND. Individuals with SSc performed worse in verbal fluency and in MMSE in comparison to adults without cognitive deficits. Verbal fluency deficits in SSc exceeded that in MiND. Performance on MMSE, COGTEL+, prospective memory, working memory, verbal fluency and concentration/attention was related to GDS scores, which did not vary across the groups. Conclusions: Patients with RA and SSc encountered cognitive dysfunction, which partially pertains to depressive symptoms. Of note, the severity of cognitive dysfunction in many cases exceeded that of MiND.