Publications by authors named "Soheila Hosseinzadeh"

6 Publications

  • Page 1 of 1

Clinical, immunological, and genetic features in 938 patients with autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED): a systematic review.

Expert Rev Clin Immunol 2021 Jun 3:1-11. Epub 2021 Jun 3.

Non-communicable Diseases Research Center, Alborz University of Medical Sciences, Karaj, Iran.

: Autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED) is a rare inborn immune error characterized by a triad of chronic mucocutaneous candidiasis (CMC), hypoparathyroidism (HP), and adrenal insufficiency (ADI).: Literature search was conducted in PubMed, Web of Science, and Scopus databases using related keywords, and included studies were systematically evaluated.: We reviewed 938 APECED patients and the classic triad of APECED was detected in 57.3% (460 of 803) of patients. CMC (82.5%) was reported as the earliest, HP (84.2%) as the most prevalent, and ADI (72.2%) as the latest presentation within the classic triad. A broad spectrum of non-triad involvements has also been reported; mainly included ectodermal dystrophy (64.5%), infections (58.7%), gastrointestinal disorders (52.0%), gonadal failure (42.0%), neurologic involvements (36.4%), and ocular manifestations (34.3%). A significant positive correlation was detected between certain tissue-specific autoantibodies and particular manifestations including ADI and HP. Neutralizing autoantibodies were detected in at least 60.0% of patients. Nonsense and/or frameshift insertion-deletion mutations were detected in 73.8% of patients with CMC, 70.9% of patients with HP, and 74.6% of patients with primary ADI.: Besides penetrance diversity, our review revealed a diverse affected ethnicity (mainly from Italy followed by Finland and Ireland). APECED can initially present in adolescence as 5.2% of the patients were older than 18 years at the disease onset. According to the variety of clinical conditions, which in the majority of patients appear gradually over time, clinical management deserves a separate analysis.
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http://dx.doi.org/10.1080/1744666X.2021.1925543DOI Listing
June 2021

Effect of methamphetamine exposure on the plasma levels of endothelial-derived microparticles.

Drug Alcohol Depend 2018 05 27;186:219-225. Epub 2018 Mar 27.

Department of Physiology, School of Medicine, Babol University of Medical Sciences, Babol, Iran.

Background: Methamphetamine (Meth), a neurotoxin, induces inflammation, oxidative stress, and triggers endothelial dysfunction and cardiovascular disease which is the second cause of death among individuals with Meth-use disorder. Oxidative stress and inflammation trigger the microparticle (MP) release. These are extracellular vesicles extracted from cell surface and identified in biological fluids. MP levels alter during pathological conditions, suggesting its potential biomarker role. In this respect, we designed the present experiment to investigate the effects of Meth on the plasma level of the endothelial-derived microparticle (EMP).

Methods: Animals received Meth (4 mg/kg i.p.) for 1, 7 and 14 days and then, the plasma level of EMPs was evaluated, using cell surface markers, including AnnexinV, CD144, CD31, CD41a antigens with the flow cytometry method. The biochemical indices and locomotor activity were also assessed in a rat model.

Results: Meth increased locomotor activity (Meth-1, 277.12 ± 20.17; Meth-7, 262.25 ± 11.95; Meth-14, 265.75 ± 14.75), inflammatory and oxidative indices as evidenced by rising of the C-reactive protein (Meth-7, 39.4 ± 1.24; Meth-14, 38.58 ± 2.19, vs 8.65 ± 0.45, mg/L) and malondialdehyde (Meth-7, 9.74 ± 1.38; Meth-14, 14.6 ± 1.45, vs 4.43 ± 0.32 nmol/L) plasma levels. We also found that Meth triggered endothelial injury, as demonstrated by elevated levels of EMP (Meth-7, 4.77 ± 0.22; Meth-14, 5.91 ± 0.34, % total events/mL) compared with control group.

Conclusion: Our data showed that Meth exposure stimulates inflammatory and oxidative pathways and facilitates the EMPs shedding. Measuring the level of EMPs might be applied as a potential diagnostic index to monitor the endothelial dysfunction in substance-use disorders.
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http://dx.doi.org/10.1016/j.drugalcdep.2018.02.015DOI Listing
May 2018

Plasma microparticles in Alzheimer's disease: The role of vascular dysfunction.

Metab Brain Dis 2018 02 5;33(1):293-299. Epub 2017 Dec 5.

Cellular and Molecular Research Center and Department of Molecular Medicine, Faculty of Advanced Technologies in Medicine, Iran University of Medical Sciences, Tehran, Iran.

Cerebrovascular lesions, a potent stimulus for endothelial cell activation, trigger cognitive and degenerative changes and contribute to pathology of Alzheimer's disease (AD). Circulating microparticles (MPs) are actively involved in the pathogenesis of AD and cerebrovascular diseases, which share common vascular risk factors. We examined the plasma changes of endothelial MPs (EMPs) and platelet MPs (PMPs) in AD patients with vascular risk factors. The plasma Annexin V CD 41a CD144 EMPs and Annexin V CD41a CD144 PMPs of 37 patients with AD, with or without vascular risk factors (hypertension, diabetes, dyslipidemia, stroke, coronary artery disease, and smoking), and 10 age-matched controls were quantified by flow cytometry. Pearson correlation analysis used to evaluate the linear relationship between variables. Significantly higher plasma levels of EMPs were observed in AD patients with vascular risk factors as compared to the patients without vascular risk factors [Mean Difference (MD): 2587.80, 95% confidence interval (CI) 770.30-4404.80], and control subjects (MD: 4990.60, 95% CI, 3054.40-6926.79). Significant correlations were found between circulating EMPs, total MPs, and PMPs. There were no significant correlations between plasma levels of EMPs/ PMPs, and cognitive decline indices. Circulating EMP levels are influenced by AD disease status, and plasma levels of MPs and PMPs are associated with vascular risk factors in patients with AD. EMP phenotyping, as cellular biomarkers of vascular injury/dysfunction, and their effects on cerebral perfusion, and cognitive decline should be further investigated. Graphical abstract Vascular endothelial cell activation results in release of endothelial-derived microparticles (EMPs), which contributing to vascular dysfunction and cognitive decline.
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http://dx.doi.org/10.1007/s11011-017-0149-3DOI Listing
February 2018

Piperine restores streptozotocin-induced cognitive impairments: Insights into oxidative balance in cerebrospinal fluid and hippocampus.

Behav Brain Res 2018 Jan 20;337:131-138. Epub 2017 Sep 20.

Neuroscience Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran; Departments of Physiology, School of Medicine, Babol University of Medical Sciences, Babol, Iran. Electronic address:

Piperine has been shown to have antioxidant activity and a cognitive-enhancing effect following long-term oral administration. In a comparative study of memantine, the current investigation threw light on the cognitive benefits of piperine. Lipid peroxidation and the ferric reducing antioxidant power (FRAP) of cerebrospinal fluid (CSF) and hippocampus in streptozotocin (STZ)-induced experimental dementia of the Alzheimer's type was measured. After reaching a criterion in a memory test, STZ-induced rats received piperine [2.5, 5, and 10mg/kg, intraperitoneally (i.p.)], vehicle, and memantine (10mg/kg, i.p.) for two weeks after the first STZ administration, or two weeks before and one week after, as a preventive approach. After the behavioral studies, samples were taken for biochemical and histological assays. An appropriate concentration of piperine (2.5mg/kg), on a daily basis, effectively increased the number of correct (non-repeated) arm entries and repressed reentry to a previously visited arm, in terms of reference errors as well as memantine (10mg/kg, i.p.), irrespective of the dose administered. The cognitive-enhancing effect induced by piperine at a relevant dose was simultaneous with CSF and hippocampal malonaldehyde decrement, and the redox balance was established to some extent by maintaining the FRAP levels of CSF near to those of the control. Similarly, the neuroprotective properties of piperine are in accordance with histopathological outcomes, which have shown an increased number of live cresyl violet (CV)-positive neurons in a dentate gyrus (DG) subregion. Therefore, the effects of piperine on the redox balance of CSF and hippocampal neurons may certainly contribute to the cognitive-enhancing activity of the drug.
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http://dx.doi.org/10.1016/j.bbr.2017.09.031DOI Listing
January 2018

Hippocampal DHCR24 down regulation in a rat model of streptozotocin-induced cognitive decline.

Neurosci Lett 2015 Feb 23;587:107-12. Epub 2014 Dec 23.

Department of Neuroscience, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran.

The DHCR24 (24-dehydrocholesterol reductase) gene codes a multifunctional protein which consists of enzymatic, antioxidant, and anti-apoptotic activities. It exists in almost all neurons and protects the neural cells against amyloid β toxicity. Several studies have shown the down regulation of DHCR24 in Alzheimer's disease. We examined the time profile of DHCR24-mRNA alteration in an animal model of streptozotocin (STZ)-induced cognitive impairment. The DHCR24 mRNA levels of hippocampus and cognitive impairment were evaluated at 7, 14, and 21 days after intracerebroventricular (ICV)-STZ/Saline administration. DHCR24 expression was down regulated at 14 and 21 days after ICV-STZ administration. The decrease in expression of DHCR24 preceded the onset of the cognitive impairment. These results suggest the potential relation between DHCR24 expression and cognitive impairment.
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http://dx.doi.org/10.1016/j.neulet.2014.12.039DOI Listing
February 2015

Elevated CSF and plasma microparticles in a rat model of streptozotocin-induced cognitive impairment.

Behav Brain Res 2013 Nov 12;256:503-11. Epub 2013 Sep 12.

Department of Neuroscience, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Alzheimer's disease (AD), can be described as a vascular disorder, is characterized by endothelial and platelet activation. One feature of activated cells is loss of lipid asymmetry, and membrane blebbing which cause microparticle (MP) formation. MPs increased under many pathological states and little information is available relating to their changes in AD. The purpose of this work was to characterize the time course of the endothelial-derived microparticles (EMPs) and platelet-derived microparticles (PMPs) alteration after intracerebroventricular (ICV) injection of streptozotocin (STZ). Rats were injected bilaterally with ICV-STZ/Saline, cerebrospinal fluid (CSF) and plasma EMPs (Annexin V(+) CD61(-)CD144(+)) and PMPs (Annexin V(+) CD61(+)CD144(-)) were analyzed with flow cytometry at 2 h, 4 h, 24 h, 4 days, 7 days, 14 days and 21 days after ICV-STZ/Saline administration. Cognitive impairment, malondialdehyde (MDA) level of hippocampus, plasma serotonin, and serum S100B were also assessed. We showed the elevation of CSF and plasma level of EMPs and PMPs, which may represent a proinflammatory and prothrombotic status. These alterations were simultaneous with the hippocampal MDA rise, plasma serotonin increment, and S100B decrement, 7 days after ICV-STZ administration and precede the onset of cognitive impairment. Understanding the profile of MP changes in CSF or plasma as biomarkers from tissues undergoing activation or damage, may be helpful in prediction or early diagnosis of AD.
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http://dx.doi.org/10.1016/j.bbr.2013.09.019DOI Listing
November 2013