Choroid plexus imaging in multiple sclerosis management - a systematic review.

INTRODUCTION: Multiple sclerosis (MS) is a central nervous system (CNS) disease associated with inflammation, demyelination, and neurodegeneration. It affects more than 2 million people globally, and usually occurs in young adults, three-quarters of whom are women. Importantly, accurate diagnosis and treatment are essential, as this disease can lead to the rapid development of disability. The choroid plexus (CP) is a structure widely known as the main cerebrospinal fluid source. However, it is also involved in immune cell trafficking to the cerebrospinal fluid, which is increased in different neurological disorders, particularly those associated with neuroinflammation. As MS is generally thought to be caused by an autoimmune process, it has been suggested that the choroid plexus may play a significant role in its pathogenesis, manifesting via changes in imaging characteristics. MATERIAL AND METHODS: Although research regarding this topic has been very limited, the results of the available studies appear promising. To further investigate this subject, we performed a systematic literature review according to the PRISMA 2020 guidelines. The PubMed and Embase databases were searched for relevant articles, and after thorough analysis, 16 studies were included in our review. RESULTS: CP volume was significantly increased in MS patients compared to healthy individuals. Furthermore, some studies found that CP enlargement occurs even before a definite diagnosis. Moreover, a few articles reported correlations between CP volume and brain atrophy, or even disease severity. CONCLUSIONS: Our findings show that CP imaging has the potential to become a novel and valuable tool in multiple sclerosis management.

Susac's syndrome diagnostic difficulties - the neurological point of view.

Susac's syndrome is a rare microangiopathy affecting small vessels of the retina, inner ear and brain. It is characterised by a triad of symptoms: encephalopathy, visual defects, and sensorineural hearing loss. The disease is probably caused by an autoimmune process. Diagnosis is based on the typical symptoms, brain MRI, and, most importantly, fluorescein angiography. It is important to distinguish between Susac's syndrome and multiple sclerosis or migraine with aura, because misdiagnosis leads to the wrong treatment. To date, no detailed guidelines for the treatment of Susac's syndrome have been developed. Immunosuppression seems to be effective. It must be remembered that early and aggressive treatment is crucial, and that delays in diagnosis, and as a result in treatment implementation, worsen the prognosis.

Variability in melatonin concentration in blood serum of patients with episodic migraine: a pilot study.

AIM OF STUDY: This study was aimed at assessing the possible effect of melatonin concentration on migraine. The serum concentration profile of melatonin in patients with diagnosed episodic migraine in the interictal period was compared to the profile in patients without migraine. Then, a correlation between the frequency and duration of migraine attacks, and the possible relationship between these parameters and melatonin levels in individual patients, was established. CLINICAL RATIONALE FOR STUDY: Melatonin secretion is related to migraine pathophysiology in many different ways. MATERIALS AND METHODS: The study was conducted in a group of 58 subjects (48 women and 10 men). The study group comprised 29 patients (24 women and five men) diagnosed with migraine according to the International Classification of Headache Disorders (ICHD-3 beta), within the framework of the Outpatient Clinic at Bielanski Hospital in Warsaw and the Clinical Department of Neurology of the 2nd Faculty of Medicine (now known as the Faculty of Medical Sciences) at the Medical University of Warsaw, Poland. The control group consisted of 29 subjects (24 women and five men) with no headache. Blood samples for the determination of melatonin were collected at midnight, 2am, 3am, 4am and 6am. Melatonin level in a frozen serum of venous blood was determined by a radio-immuno-enzymatic method at the Department of Histology and Embryology of the Faculty of Veterinary Medicine at the University of Warmia and Mazury in Olsztyn, Poland. RESULTS: No statistically significant differences between the levels of melatonin and the averaged advances of melatonin profiles were observed in the examined and the control group. There were demonstrated medium negative correlations between the maximum value of melatonin and the duration of migraine (R = -0.4, p = 0.03). There were also observed statistically significant differences (p = 0.01) between the averaged advances of melatonin profiles, depending on the duration of migraine. CONCLUSIONS AND CLINICAL IMPLICATIONS: Our study showed no abnormalities of melatonin secretion in patients with migraine during the interictal period. The results of studies available in the literature depend on the nature of the headache (episodic or chronic) and the time of measuring the concentration of melatonin (during a headache attack or in an interictal period).

Cerebral venous and sinus thrombosis diagnosis: preliminary study of clinical picture and D-dimer concentration correlation.

AIM OF THE STUDY: We investigated whether D-dimer (DD) concentration is elevated in cerebral venous and sinus thrombosis (CVST), as has been reported in the literature. CLINICAL RATIONALE FOR THE STUDY: CVST is a disease with variable clinical presentations and a challenging diagnosis. We looked into whether D-dimer concentration might be an indicator of CVST, and the need for neuroimaging tests correlated with clinical factors. MATERIALS AND METHODS: We included all consecutive patients (mean age 41.6 years) with CVST treated in our neurology department from 2014 to 2018 whose DD levels had been measured. DD concentrations were categorised as normal (≤ 0.5 µg/ml) or elevated ( > 0.5 µg/ml). Appropriate imaging confirmed the diagnosis of CVST. The results were compared to those of a control group consisting of 22 age- and sex-matched patients (mean age 40 years) with a diagnosis of primary headache (tension type or migraine) hospitalised to exclude secondary causes. RESULTS: In 20 patients in the CVST study group, median level of DD was 1.0 + 0.57 µg/ml (range 0.19-2.45 µg/ml), compared to the control group's mean DD level of 0.50 + 0.45 µg/ml (range 0.15-1.73 µg/ml), with p < 0.005. Higher DD levels were associated with complications of the disease and fatal course (p < 0.005). One female and one male patient died because of CVST with DD levels of (respectively) 2.45 and 1.80 µg/ml - the two highest concentrations in our study group. CONCLUSIONS AND CLINICAL IMPLICATIONS: DD concentration, especially in headache patients, may be a factor to predict CVST and an indicator for further diagnostic procedures with venography. But in clinical practice, low levels of DD cannot be taken to exclude CVST.

Neuroendocrine aspects of anorexia nervosa and bulimia nervosa.

Endocrine dysfunctions in eating disorders (anorexia nervosa, bulimia nervosa) result from disturbed regulation of hypothalamo-pituitary-gonadal, hypothalamo-pituitary-adrenal, hypothalamo-pituitary-thyroid and hypothalamo-pituitary-GH-IGF1 axes as well as of altered peripheral endocrine metabolism. Some peptides of hypothalamic origin, as well as those secreted by the adipose tissue and gastrointestinal tract including pancreatic hormones, are involved in the control of appetite and satiety. These peptides play also an important role in the mechanism of hormonal secretion. Altered activity of these biologically active substances may lead to the disturbances in the regulation of energy and hormonal homeostasis.

Evaluation of activities of daily living in patients with slowly progressive neuromuscular diseases.

Slowly progressive neuromuscular diseases include but are not limited to: facioscapulohumeral muscular dystrophy (FSHD) and limb-girdle muscular dystrophy (LGMD), hereditary motor and sensory neuropathy (HMSN) and spinal muscular atrophy type III (SMA3). The purpose of this study is to present an evaluation of basic and complex activities of daily living in patients suffering from these diseases. The study was conducted on a group of 58 Polish patients: 25 patients with HMSN, 19 with LGMD and FSHD and 14 with SMA3. The research instrument consisted of two parts: a specially designed questionnaire and Nottingham Extended ADL Index. The survey was voluntary, anonymous and self-administered. In our study the highest scores on the NEADL scale were achieved by HMSN patients, and the lowest by patients with SMA3. The research revealed statistically significant differences between all the groups in the total number of points achieved on NEADL scale. The study revealed that for most respondents the most difficult tasks were those in the area of 'mobility'. It is consistent with reports in the literature, which confirm that out of the slowly progressive neuromuscular diseases included in this research, SMA3 is a disease leading to the biggest limitations in performing the activities of everyday life.

Aspirin Action in Endothelial Cells: Different Patterns of Response Between Chemokine CX3CL1/CX3CR1 and TNF-α/TNFR1 Signaling Pathways.

PURPOSE: TNF-α induces fractalkine (CX3CL1) and its receptor CX3CR1 in endothelial cells through NF-қB activation. NF-қB inhibitors may reduce the expression of CX3CL1, and modulation of the CX3CL1/CX3CR1 signaling was proposed as a new target for aspirin. We examined the effects of aspirin on CX3CL1 and TNF-α production, as well as CX3CR1 and TNFR1 expression. METHODS: HUVECs isolated after term pregnancies (N = 28) were cultured in vitro. Lipopolysaccharide (1 µg/ml) was used as CX3CL1 inducer. HUVECs were exposed to six different concentrations of aspirin (between 1.0 and 6.0 mM) during 7 days. The levels of CX3CL1 and TNF-α in the culture media were measured using ELISA. After termination of the cultures, mean expressions of CX3CR1 and TNFR1 were examined in the immunostained paraffin sections using quantitative immunohistochemistry. RESULTS: Aspirin significantly (p < .05) decreased CX3CL1 production, and the mean decrease in CX3CL1 production was inversely proportional to increased (p < 0.05) expression of CX3CR1. The combined mean CX3CL1 concentrations, including all time points, equaled 782.18 ± 74.4 pg/ml in aspirin treated HUVECs compared to a total concentration of 2467.53 ± 127.5 pg/ml combined from the respective time points in the controls. An inhibition of TNF-α production in HUVECs after pretreatment with aspirin was observed. Unlike in the case of CX3CR1 expression, there were no signs of TNFR1 upregulation. CONCLUSIONS: Autoregulation between CX3CL1 and CX3CR1 may explain overexpression of CX3CR1 as the compensatory effect in aspirin-treated HUVECs. Inhibition of CX3CR1 could prevent thrombotic complications in the early period after discontinuation of aspirin.

Assessment of plasma brain-derived neurotrophic factor (BDNF), activity-dependent neurotrophin protein (ADNP) and vasoactive intestinal peptide (VIP) concentrations in treatment-naïve humans with multiple sclerosis.

OBJECTIVE: Multiple sclerosis (MS) is a chronic disease of the central nervous system (CNS) characterized by coexisting processes of inflammation, demyelination, axonal neurodegeneration and gliosis. Autoimmune processes play a pivotal role in the disease. The immune system may be modulated by neurotrophins and neurotrophin factors. Aim of the study was to assess plasma levels of brain-derived neurotrophic factor (BDNF), activity-dependent neurotrophin protein (ADNP) and vasoactive intestinal peptide (VIP) in treatment-naïve humans with newly diagnosed multiple sclerosis. We also elucidated the potential influence of selected inflammatory agents on peripheral concentration of BDNF and ADNP. MATERIAL AND METHODS: The study population comprised of 31 untreated patients with MS and 36 controls from a single hospital centre. Assessment of BDNF and ADNP was performed with use of ELISA methods. VIP was measured with RIA. Selected cytokine levels (IL 6, IL 10, and TNF α) were evaluated with ELISA tests. Statistical analyses were performed. RESULTS: We failed to find any significant differences between ADNP, BDNF, VIP, CRP levels and concentration of cytokines between individuals with MS and the controls. No correlation was observed between ADNP, BDNF and VIP as the first parameter and CRP, IL 6, IL 10, TNFα levels and the Expanded Disability Status Scale score in MS. CONCLUSIONS: Newly diagnosed, treatment-naïve patients with MS have comparable levels of plasma BDNF, ADNP and VIP to those of healthy controls.

CX3CL1 (fractalkine) and TNFα production by perfused human placental lobules under normoxic and hypoxic conditions in vitro: the importance of CX3CR1 signaling.

OBJECTIVE: Inflammation and hypoxia activate the fractalkine (CX3CL1) receptor (CX3CR1)-related signaling pathway. Tumor necrosis factor alpha (TNFα) induces CX3CL1, influencing a mechanism of CX3CL1 autoregulation by CX3CR1 expression. We compared spontaneous and lipopolysaccharide (LPS)-induced CX3CL1 and TNFα production by human placenta under normoxic vs. hypoxic conditions, with respect to CX3CR1 expression and its functional status. METHODS: Placental lobules of term placentae (N = 24) were perfused extracorporeally. CX3CL1 and TNFα concentrations were measured in the perfusion fluid by ELISA. LPS, anti-CX3CR1 antibodies and pirfenidone were used in respective subgroups. After perfusion, CX3CR1 expression was estimated in placental tissue using quantitative immunohistochemistry, and the final results were adjusted for the mean microvascular density. RESULTS: The highest increase in CX3CL1 concentration in response to LPS was observed in hypoxia (p < 0.05). Unlike in normoxia, anti-CX3CR1 administration in hypoxia significantly reduced the LPS-evoked response. CX3CR1 expression was augmented by hypoxia and reached 260.9 ± 41 (% ±SEM) of the reference value in normoxia. Positive immunostaining for CX3CR1 corresponded to the vascular endothelium. Pirfenidone inhibited hypoxia + LPS-related increase in TNFα production and prevented the up-regulation of CX3CR1. CONCLUSION: The modulatory influence of TNFα on CX3CR1 expression in hypoxia and CX3CL1/CX3CR1 interaction may serve as a compensatory mechanism to preserve or augment the pro-inflammatory course of intercellular interactions in placental endothelium.

Plasma chemerin levels in patients with multiple sclerosis.

OBJECTIVES: Chemerin, a novel adipokine produced by adipose tissue and liver, is associated with markers of metabolic syndrome, and additionally, acting as chemoattractant for cells of immune system it may regulate immune cell properties. MATERIAL AND METHODS: In order to evaluate plasma chemerin concentration in multiple sclerosis (MS) individuals we investigated 39 MS patients (among them 23 subjects were lean and 16 were overweight or obese) and 42 controls with tension headaches (29 of them were lean and 13 were overweight or obese). All patients had a brain MRI scan with gadolinium contrast as well as an assessment of the presence of oligoclonal bands in cerebrospinal fluid (CSF) and estimation of the CSF IgG index. The neurologic status was evaluated with use of the Expanded Disability Status Scale. Chemerin levels in plasma were measured using ELISA kit. Lipid profile, glucose and insulin levels, CRP and selected cytokine concentrations were also determined. RESULTS: Plasma chemerin concentrations in overweight/obese MS subjects were higher when comparing to lean MS individuals and the controls, both from lean and overweight/obese subgroups. Significant difference was found between the results of overweight/obese MS and lean controls. CONCLUSIONS: An increase of chemerin levels in patients with multiple sclerosis is associated with overweight and obesity.

Fractalkine (CX3CL1) and its receptor CX3CR1 may contribute to increased angiogenesis in diabetic placenta.

Chemokine CX3CL1 is unique, possessing the ability to act as a dual agent: chemoattractant and adhesive compound. Acting via its sole receptor CX3CR1, CX3CL1 participates in many processes in human placental tissue, including inflammation and angiogenesis. Strongly upregulated by hypoxia and/or inflammation-induced inflammatory cytokines secretion, CX3CL1 may act locally as a key angiogenic factor. Both clinical observations and histopathological studies of the diabetic placenta have confirmed an increased incidence of hypoxia and inflammatory reactions with defective angiogenesis. In this study we examined comparatively (diabetes class C complicated versus normal pregnancy) the correlation between CX3CL1 content in placental tissue, the mean CX3CR1 expression, and density of the network of placental microvessels. A sandwich enzyme immunoassay was applied for CX3CL1 measurement in placental tissue homogenates, whereas quantitative immunohistochemical techniques were used for the assessment of CX3CR1 expression and the microvascular density. Significant differences have been observed for all analyzed parameters between the groups. The mean concentration of CX3CL1 in diabetes was increased and accompanied by augmented placental microvessel density as well as a higher expression of CX3CR1. In conclusion, we suggest involvement of CX3CL1/CX3CR1 signaling pathway in the pathomechanism of placental microvasculature remodeling in diabetes class C.

Plasma NPY concentrations in women with acute ischemic stroke.

OBJECTIVE: It has been reported that plasma NPY levels were increased in obesity, type 2 diabetes mellitus and hypertension. The symptoms of metabolic syndrome frequently appear in patients with acute ischemic stroke. The association between plasma NPY levels and metabolic markers in women with acute ischemic stroke was investigated in the current study. METHODS: Plasma NPY concentrations were determined using radioimmunoassay in 58 women aged 60-85 (mean age: 76.5±0.8) with acute ischemic stroke and in 24 women aged 63-67 (mean age: 65.6±0.6) of the control group. Stroke was defined according to the NIHSS (National Institute of Health Stroke Scale) and was confirmed using CT or MR scan. RESULTS: The prevalence of type 2 diabetes, hypertension and insulin resistance was higher in the group of patients with stroke. Plasma NPY levels measured during the 1st day and 10 days after the acute phase of stroke were significantly lower (p<0.001) compared to the control group. CONCLUSION: In women with acute ischemic stroke plasma NPY concentrations were decreased in spite of higher frequency of the occurrence of the symptoms of metabolic syndrome.

Insulin-like growth factor 1 and its prognostic value in the course of acute ischemic cerebrovascular events.

Introduction: The aim of the study was to evaluate insulin-like growth factor 1 (IGF-1) as a predictor of the course of an acute cerebral ischemic event (AICE). This polypeptide, by activating receptors that are present in most tissues, including the brain, mediates the anabolic activity of growth hormone (GH) and its impact on growth and maturation processes, as well as organisms' survival time. AICE can occur in the form of a transient ischemic attack (TIA) or an ischemic stroke (IS). Material and methods: The study included 86 participants. The correlation between serum IGF-1 concentration and the clinical status of 56 patients on days 1 and 9 of AICE, as well as risk factors and the course of the disease, were prospectively analyzed. The control group consisted of 30 healthy volunteers. Results: Patients with a minor baseline neurological syndrome had higher serum IGF-1 concentrations than patients with severe baseline neurological dysfunctions. Multidimensional analyses showed that high IGF-1 values independently determined the worse course of the disease, especially in patients with a severe neurological deficit present on the first day of AICE. Conclusions: Our results indicate that the high level of circulating IGF-1 on the first day of AICE is an independent factor determining the unfavorable course of the stroke, and this relationship is proportional to the severity of the baseline neurological deficit. The study also revealed a positive correlation between the decreased plasma IGF-1 concentration on the first day of AICE and the severity of neurological symptoms.

Overactivity of the Less Affected Side as a Possible Pattern of Asymmetry in Sitting in Patients Suffering from First-Time Ischemic Stroke-An Observational Study.

It has been observed that in some people in the acute phase of ischemic stroke (IS) there is a tendency to shift the body weight towards the side more affected by the disease and a tendency to spontaneous movements of the upper and/or lower limbs (not covered by the neurological syndrome). The purposes of this study were: to define the kind of behavior observed, and to select symptoms which can predict its occurrence. Participants (n = 222) hospitalized due to first-time IS were assigned to three groups. A: 78 patients with no lateralization of the neurological syndrome (lateralization of the neurological syndrome-LoNS); B: 109 patients with LoNS; O+ group: 35 patients, who at the beginning of hospitalization presented, apart from LoNS, characteristic motor symptoms performed by the less affected side. Patients underwent therapy depending on the neurological symptoms. If the patient showed potential symptoms of a new phenomenon, overactivity of the less affected side (OLAS), a trial therapy (focused on this behavior) was used to confirm it. The predictive symptoms, selected among these from the index day, for the occurrence of OLAS in sitting were distinguished: asymmetry in supine posture and simple, repetitive movements of the nonparetic upper extremity.

Resistin levels in women with ischemic stroke.

OBJECTIVES: Resistin may be an independent inflammatory marker of atherosclerosis. Therefore, its circulating level might be important prognostic factor of cardiovascular disease in humans. We aimed in this study to assess plasma resistin concentration in Polish women with acute ischemic stroke, who additionally suffer from chronic diseases: diabetes, hypertension and/or obesity. The changes of resistin levels after 10 days from the onset of stroke and possible associations between resistin and pro-inflammatory cytokine TNFα were also evaluated. MATERIAL AND METHODS: Material consisted of 41 women with ischemic stroke (aged 60-85 years) and 64 controls (aged 60-85 years). Circulating resistin and TNFα concentrations were measured using ELISA. Blood was taken twice in the stroke group, in the first and tenth day from the onset of clinical symptoms, and only once in the controls. Clinical and biochemical data (blood pressure, weight, height, glucose, insulin, lipid profile) were collected. RESULTS: Higher concentrations of resistin and TNFα were observed in ischemic stroke patients at the first day comparing to the controls. Second evaluation after 10 days in comparison with the first measurement revealed significantly higher TNFα levels and non-significant lower values of resistin. Resistin positively correlated with TNFα and stroke severity. CONCLUSIONS: Changes in resistin and TNFα concentrations were observed in the course of stroke. Further investigations are required to assess the implication of these findings. Higher resistin concentration might be associated with worse neurological deficits.

Decreased total serum adiponectin and its isoforms in women with acute ischemic stroke.

OBJECTIVE: An association between cerebral infarct risk factors and serum adiponectin levels (both total and separate isoforms) has previously been identified. The aim of this study was to assess circulating levels of all forms of adiponectin in the course of an ischemic stroke. MATERIAL AND METHODS: Adiponectin and its isoforms (HMW, MMW and LMW) were measured in serum samples taken from 38 women in the first 24 hours of cerebral infarct and 38 controls matched for gender, body mass index (BMI) and age. In addition, biochemical parameters (glucose, insulin, lipid profile) and clinical data (blood pressure, weight, and height) were evaluated. RESULTS: A significant reduction in serum levels of adiponectin and all examined fractions of this adipokine was observed in women suffering from acute ischemic stroke, compared with the matched controls. CONCLUSIONS: Differences in the serum adiponectin array between stroke subjects and controls were identified and further studies are required to investigate the clinical implications of this finding.

Secondary Impact of COVID-19 Pandemic on People with Parkinson's Disease-Results of a Polish Online Survey.

The COVID-19 pandemic causes increased mental stress and decreased mobility, which may affect people with Parkinson's disease (PD). The study aimed to investigate the secondary impact of the COVID-19 pandemic on the level of activity, quality of life (QoL) and PD-related symptoms. The respondents completed an online survey in Polish in the period from December, 2020 to June, 2021. The questionnaire was completed by 47 participants aged 43 to 90 years (mean 72.1 ± 1.3 years). A total of 94% reported reduced contact with family and friends. Over 90% remained active during the pandemic. However, 55% of people with PD showed subjectively lower level of activity then before the pandemic. Moreover, 36% of the respondents felt afraid to visit a doctor and reported problems with access to medication. Subjective QoL reduction was reported by 80%, and 83% declared worsening of PD symptoms. The post pandemic deterioration of motor symptoms in people with PD did not affect their QoL. However, the deterioration of contacts and feelings of isolation had a significant impact on the decline in quality of life (p = 0.022 and p = 0.009, respectively) and the presence of anxiety (p = 0.035 and p = 0.007, respectively). These results may indicate than greater importance of social and mental factors than fitness and health-related factors in the QoL self-assessment of the people with PD.

The metabolic, neuroprotective cardioprotective and antitumor effects of the Klotho protein.

Klotho is a transmembrane protein with a wide spectrum of activity. The human Klotho gene shows 86% amino acid identity with the mouse protein. Many important pleiotropic functions of the Klotho protein have been revealed. Amongst them, there is a regulation of nitric oxide production, suppression of oxidative stress and inflammation, influence on the insulin-like growth factors and fibroblast growth factors signaling, modulation of calcium and phosphate metabolism, synthesis of vitamin D and other. Two forms of the Klotho protein are known. The secreted form strongly inhibits the oxidative stress, and, in humans, is more dominant than the membrane form. Studies on a mouse model resulted in the finding of the anti-aging effect of the Klotho protein. This activity is mainly associated with the suppression of oxidative stress, as well as it could be related to neuroprotective, cardioprotective, and metabolic functions.It might be speculated that Klotho, regarded as a neuroprotective factor, may have therapeutical applications in the future in the treatment of demyelinating and neurodegenerative disorders, especially multiple sclerosis (MS) and Alzheimer's disease (AD). The Klotho through inhibition of oxidative stress possesses cardioprotective properties. Of note, one functional variant of Klotho is a risk factor for coronary disease as well as some nucleotide polymorphisms are associated with carotid arteriosclerosis. Moreover, the Klotho protein can inhibit Angiotensin II-induced cardiomyocyte hypertrophy. All those effects indicate that the Klotho protein may be useful in the therapy of heart failure and hypertension. Undoubtedly, metabolic disturbances play an important role in the pathogenesis of many neurodegenerative and cardiovascular diseases. The metabolic effects of the Klotho protein are strongly connected with its neuroprotective and cardioprotective activity. This protein affects adipogenesis, metabolism of glucose and lipids as well as calcium-phosphate system by influence on the activity of fibroblast growth factors (FGF19, FGF23, FGF21). Finally, it has been revealed that the Klotho protein has antitumor activity. Besides, the FGF-Klotho system may have a role in longevity and aging-related disorders.

Peripheral levels of selected adipokines in patients with newly diagnosed multiple sclerosis.

INTRODUCTION: Multiple sclerosis (MS) is an autoimmune disease of the central nervous system. The exact aetiology is unknown. However, genetic and environmental factors are suggested to be involved in the pathogenesis of MS. Improper diet, resulting in obesity and metabolic syndrome, can contribute to this disease. Adipokines, secreted by adipose tissue, link the metabolism and immune system. MATERIAL AND METHODS: We aimed to assess plasma levels of selected adipokines in newly diagnosed, treatment-naïve individuals with multiple sclerosis. Our group comprised 58 individuals (31 MS patients and 27 controls, matched for age and BMI) without diabetes, hypertension, or dyslipidaemia. Circulating adiponectin and all adiponectin fractions, visfatin, and omentin concentrations were measured. Metabolic parameters were also assessed. RESULTS: In MS individuals we observed the following results: higher concentrations of visfatin, lower levels of omentin, and no differences in adiponectin array. There were also correlations between some adipokines and metabolic parameters. After adjustment to BMI, a significant decrease in total adiponectin, high-molecular weight (HMW) adiponectin and omentin, and an increase in medium-molecular-weight (MMW) adiponectin were observed in the group of MS patients when compared to those of the controls. CONCLUSIONS: Our results indicate that adiponectin with its fractions, visfatin, and omentin cannot be considered as causative factors in the early phase of multiple sclerosis. However, the potential role of adipokines in MS is possible because they might be involved in the pathogenesis of MS, regarded as an autoimmune disorder.

Copeptin - a new diagnostic and prognostic biomarker in neurological and cardiovascular diseases.

Copeptin, arginine vasopressin (AVP)-associated 39 aminoacid glycopeptide, is a C-terminal part of pro-AVP. AVP acts through V1a, V1b, and V2 receptors. The effect on V1a receptors is connected with arterial vasoconstriction, on V2 with antidiuretic action, and on V1b with the secretion of ACTH, insulin, glucagon. Copeptin is found in the circulation in equimolar amounts with AVP. It is a very stable peptide and easy to estimate. Copeptin is a good diagnostic marker in many disorders in which vasopressinergic dysfunction plays a role in pathogenesis such as a polyuria-polydipsia syndrome, neurological disease (ischemic stroke, nontraumatic, intracerebral hemorrhage, aneurysmal subarachnoid hemorrhage and neurodegenerative disease (multiple sclerosis). Copeptin is a diagnostic and prognostic marker in cardiovascular diseases like heart failure (HF) and acute myocardial infarct (AMI). Copeptin is a sensitive diagnostic marker in the early stage of AMI especially in patients with non-ST segment elevation and post AMI complications. Copeptin is also an important diagnostic and prognostic marker in metabolic diseases (diabetes mellitus, metabolic syndrome, insulin resistance), connected with some neurological and cardiovascular diseases. In the future, these findings may have also therapeutic applications in conditions where the AVP receptor antagonist therapy is appropriate.