The aim: To research differences of interleukin (IL)-17 and IL-23 serum levels in patients with Alzheimer’s disease, vascular dementia and mild cognitive impairment. Material and methods: Serum levels of IL-17 and IL-23 were measure by ELISA for 15 patients with Alzheimer’s disease, 14 with vascular dementia, 30 with mild cognitive impairment and 30 control individuals without cognitive impairment. Results: Serum concentrations of IL-17 were significantly higher in Alzheimer’s disease patients (P=0.0023) than control, in vascular dementia no significant differences(P=0.4154). Level of IL-23 was significantly higher than control in Alzheimer’s disease patients (P=0.0170) and vascular dementia (P=0.0002), but in Alzheimer’s disease it was in 12.5 time higher. In total mild cognitive impairment patients no significant differences in interleukin concentration with control, but significant differences observed for amnestic form in IL-17 (P=0.0436) and IL-23 (P=0.0019). Conclusions: IL-17 and IL-23 level significant higher in Alzheimer’s disease patients compared with control and vascular dementia. From mild cognitive impairment levels of detectable interleukins was higher in amnestic form that may be early marker of progression in Alzheimer’s disease.

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Alzheimer's disease (AD) is a degenerative disease that leads to dementia symptoms [1, 2]. Histopathological signs of AD are amyloid plaques in the brain, mainly consisting of fibrillary forms of amyloid β-peptide-40 (Aβ-40) and amyloid β-peptide-42 (Aβ-42). Neutrophils are the main targets for IL-17 in the central nervous system (CNS) that promote inflammation and damage to CNS tissues, and may play an important role in the development of AD pathology. Interleukin 23 (IL‑23) synergizes with IL-6, IL-1 and is involved in the differentiation of Th17 cells in a pro-inflammatory context. The aim of the study was to analyze the relationship between interleukin levels of IL-17, IL-23 and neurocognitive scales in patients with AD, vascular dementia (VD) and mild cognitive disorder (MCD). The study involved 89 patients, of which 59 patients had cognitive impairment (32 men and 27 women, mean age 66.8±8.4 years); among them, 29 had major neurocognitive impairment (NCD), including 15 patients with AD, 14 – with VD, 30 patients – with MCD and 30 people in the control group had no cognitive deficit. All patients were tested with comprehensive neuropsychological examination using the following tests and scales: Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), Frontal Assessment Battery (FAB), Alzheimer Disease Assessment Scale-cognitive (ADAScog). Serum levels of cytokines of IL-17 and IL-23 were assayed using sandwich ELISA on «Chem Well 2900» immunoanalyzer (Awareness Technology, USA). Test systems using Bender Medsystems, Australia (IL-17 and IL-23) were used in accordance with the manufactures instructions. Levels of detectable interleukins (IL-17 and IL-23) were significantly higher in patients with AD vs. patients with VD and MCD. The correlations between the two cytokines and the MMSE scales, MoCA, ADAS-cog and FAB were examined. Our results showed a significant positive correlation between the serum concentration of IL-23 and neurocognitive scales in all patients with AD. The most relevant correlations in the AD group were linked with the scales: ADAS-cog (r = 0.760; р = 0.001), namely with the sections «tasks for repeating words» (r = 0.775; p ˂ 0.001), «constructive praxis» (r = 0.651; p = 0.010), «orientation» (r = 0.684; p = 0.01), as well as «word recognition tasks» (r = 0.616; p = 0.020); and with MoCA scale (r = −0.592; p = 0.020), namely with the section «delayed recall» (r = −0.641; p = 0.010). A significant positive correlation was established between IL-23 and individual sections of the ADAS-cog scale in patients with MCD (r = 0.423; p = 0.020), namely with «word recognition tasks» (r = 0.466; p = 0.030), «understanding» (r = 0.306; p = 0.059) as well as «strike out numbers» (r = 0.301; p = 0.061). A weak positive correlation was found between the serum concentration of IL-23 and ADAS-cog scores in patients with VD (r = 0.497; p = 0.045). Moderate positive correlation was observed for IL-23 with «concentration and distraction» (r = 0.558; p = 0.040). An inverse correlation was established between the serum levels of IL-23 and MoCA scores in patients with VD (r = −0.510; р = 0.060), especially with «language» (r = −0.538; p = 0.047) and «executive functioning» (r = −0.485; p = 0.079). However, no other significant correlations were found between the serum concentration of IL-17 and neurocognitive domains in patients with MCD and VD. Correlation analysis confirmed the relationship between the severity of cognitive impairment and the level of proinflammatory markers, suggesting that inflammation can lead to cognitive decline in AD patients. The results of the study indicated that IL-23 may have a more complex relationship with the progression of this disease which gives reason to consider IL-23 as a marker of inflammatory activity. Levels of detectable proinflammatory cytokines (IL-17 and IL-23) were significantly higher in patients with AD vs. patients with VD and MCD. Such more pronounced changes in the production of interleukin 23 in patients with AD may indicate the activity of the inflammatory process. The level of IL-23 in all examined patients with Alzheimer's disease had high correlations with indicators of neurocognitive scales, which indicated its important role in the pathogenesis of this disease. There were no other significant correlations between the serum concentration of IL-17 and neurocognitive domains in patients with MCD and VD.

Comorbid and co-occurring diseases are risk factors for the progression of episodic migraine to chronic migraine. Biomarkers for migraine could help with diagnosis and treatment selection and monitoring. Aim. To examine the role of the plasma level of calcitonin-gene-related peptide (CGRP) in the diagnosis of episodic migraine in combination with comorbid conditions in the form of cervicalgia and psychoemotional disorders. Materials and methods. The study included 112 patients (84 women, 28 men; mean age 18-58 years), episodic migraine with typical aura – 17, without aura – 60. Patients were divided into 3 groups: I – episodic migraine with cervicalgia (n = 42), II – episodic migraine only (n = 35), III – cervicalgia only (n = 35). The Visual Analogue Scale, Migraine Disability Assessment (MIDAS) score, Headache Impact Test (HIT-6), Neck Disability Index, State-Trait Anxiety Inventory, Beck’s Depression Inventory and the number of days with headache were assessed. The control group consisted of 30 healthy persons to compare the level of CGRP. The serum level of CGRP was determine by enzyme-linked immunosorbent assay using the sandwich ELISA principle. Results. Plasma level of CGRP was higher in groups I and II compared with group III (P = 0.012543), where it did not differ from the control (51.48 ± 5.08 pg/ml). The highest level of CGRP was observed in group I (242.98 ± 5.08 pg/ml) in comparison with group II (145.82 ± 15.38 pg/ml, P = 0.000341). Co-occurring neck-pain in patients with episodic migraine was associated with mood and anxiety disorders. Migraine severity, according to the MIDAS score, was most significantly influenced by plasma level of CGRP, severity of subjective and objective symptoms of headache by the HIT-6, level of State-anxiety and Trait-anxiety, number of days with headache during the last 3 months. Conclusions. The serum level of CGRP is a reliable diagnostic and differential diagnostic laboratory biomarker for episodic migraine. Additional painful syndrome such as cervicalgia influences CGRP level and daily activity, mood and anxiety disorders in episodic migraine patients.

Background. Systemic cancer and stroke are the most common diseases and the frequent death factors in older people worldwide. The relationship between cancer and stroke is complex, since cancer leads to an increased risk of stroke through specific pathophysiological mechanisms. Purpose. Analyzing possible mechanisms of development of cancer-associated stroke, strategies of diagnosis and treatment. Materials and methods. The contributions were selected based on PubMed (https://pubmed.ncbi.nlm.nih.gov/), Clinical Key Elsevier (https://www.clinicalkey.com), Cochrane Library (https://www.cochranelibrary.com/) and GoogleScholar (https://scholar.google.com/) databases published from 2012 to 2022, dealing with cancer-associated stroke. Results and discussion. There are several underlying pathophysiological mechanisms of cancer-associated stroke, which may be directly related to cancer or caused by cancer complications. The most common ones are intravascular cancer coagulopathy, non-bacterial thrombotic endocarditis, a direct impact of the tumor on the vascular system or therapeutic and diagnostic interventions for the treatment of cancer that is chemotherapy, radiation therapy complications, as well as activation of the usual mechanisms of stroke, atherosclerosis in particular. The risk of stroke is also related to cancer aggressiveness. The characteristic features of cancer-associated stroke which is related to cancer coagulopathy are multiple lesions in various arterial areas, as well as laboratory data indicating coagulopathy in the form of increased level of D-dimer, elevated C-reactive protein, low hematocrit. Conclusions. Cancer leads to an increased risk of stroke due to specific pathophysiological mechanisms. These mechanisms are multiple and complex, but the most well-known and widespread is cancer intravascular coagulopathy, which has specific laboratory biomarkers. Numerous studies continue investigating the factors associated with coagulopathy in stroke patients, cancer characteristics, and evaluation of biological markers of stroke-causing intravascular coagulopathy, as well as monitoring the effects of anticoagulation therapy in patients with cancer-associated stroke.