E. Koutsouraki

Aristotle University of Thessaloniki, Saloníki, Central Macedonia, Greece

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Publications (97)181.21 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: We examined the sera of 103 demented patients of a mean age of 75 years and 60 age-matched healthy individuals, using ELISA, to investigate the levels of IgM antibodies against GM1, GD1b, and GQ1b gangliosides and their possible correlation with clinical parameters (age, severity, and type of dementia). All the individuals that demonstrated positive titers of anti-ganglioside antibodies were demented patients whereas normal controls showed borderline or negative values. Significant correlation was revealed between IgM anti-GM1 and both the age of the patients and the severity of dementia. Most of the patients with increased IgM anti-GD1b titers suffered from AD.
    No preview · Article · Jun 2014 · Journal of Alzheimer's disease: JAD
  • E Hatzifilippou · E Koutsouraki · V G Costa · S J Baloyannis
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    ABSTRACT: Background: Increasing evidence suggests that gangliosides act as important mediators in both de- and remyelination. The scope of the present research was to investigate the presence of immunoglobulin (Ig) M antibodies against GM1, GD1b, and GQ1b gangliosides in the sera of patients with dementia and the possible connection with clinical parameters of the disease. Method: This research topic demonstrates the investigation of 103 patients with dementia and 60 healthy individuals using enzyme-linked immunosorbent assay for the presence of 3 antiganglioside antibodies in their sera. Results: The authors report a positive connection between IgM anti-GM1 and the age (P = .005) and the severity of dementia (P = .005). Most of the patients who revealed increased IgM anti-GD1b levels had Alzheimer's disease (AD; P = .002). Conclusion: This study indicates that elevated IgM anti-GM1 may be connected with the neurodegeneration in older patients with severe dementia and that AD may also be associated with increased IgM anti-GD1b levels.
    No preview · Article · May 2014 · American Journal of Alzheimer s Disease and Other Dementias
  • Euphrosyni Koutsouraki · Dimitrios Michmizos

    No preview · Article · Sep 2013 · Multiple Sclerosis
  • Marta Sochocka · Euphrosyni S. Koutsouraki · Kazimierz Gąsiorowski · Jerzy Leszek

    No preview · Article · Aug 2013 · CNS & Neurological Disorders - Drug Targets (Formerly Current Drug Targets - CNS & Neurological Disorders)
  • Source
    Euphrosyni Koutsouraki · Aikaterini Fotakidou · Thalia Kalatha · Stavros Baloyannis
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    ABSTRACT: The epidemiologic profile of multiple sclerosis (MS), one of the most common diseases of the central nervous system, is not well defined in northern Greece. We analyzed retrospectively the records of the MS patients admitted in our Neurology Department, between the years 1979-2008. We studied a total of 1180 MS patients, with an average annual rate of 39 ± 11.8 MS patients, demonstrating a female to male ratio of 1.6:1. The estimated prevalence of MS in Thessaloniki, the largest city in northern Greece, on December 31 2008, was 57:100,000 placing the area in the high-risk zone while it was 6,8:100,000 on December 31, 1981, in the medium-risk zone. The mean age during the exacerbation of the disease was 28 ± 9 years for females and 31 ± 8 years for males, with significant difference between means (t = 5,8, p < 0,001). The average annual rate of attacks was 1.6 ± 0.7 per 100.000 population. Patients' admissions was significantly less in winter with comparison to the other seasons (t = 3, p = 0,002). As far as monthly distribution, the maximum number of admissions was noted in May (121 patients, 10.25%) and September (118 patients, 10%) and the minimum in December (58 patients, 4.9%). Our study indicates an increase of the incidence of MS in northern Greece, central Macedonia prefecture and mainly in the city of Thessaloniki, during the last 30 years.
    Full-text · Article · May 2013
  • Euphrosyni Koutsouraki · Dimitrios Michmizos · Thalia Kalatha · Stavros Baloyannis
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    ABSTRACT: We present the case of a 14-year-old Caucasian female, with intracranial hemorrhage due to an extensive brainstem cavernous hemangioma, asymptomatic until the date of her admission. Further investigation revealed multiple brain cavernous hemangiomas with two supratentorial hemangiomas demonstrating signs of past bleeding, a cervical vertebral dysplasia (Klippel-Feil type II) and nephrolithiasis, in addition to her history of polycystic ovaries and impaired glucose tolerance, all together presenting a novel clinical combination. We are describing the management of such a patient, according to our current knowledge, inquiring into the possible connections between the conditions detected, as well as, discussing the questions that arise from this rare case.
    No preview · Dataset · Apr 2013
  • Euphrosyni S Koutsouraki · John J Anastasiades · Stavros J Baloyannis
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    ABSTRACT: The aim of our investigation was to demonstrate the wide distribution of glutamate N-methyl-D-aspartate receptors (NMDA R), particularly the not-widely investigated 2A and 2B subunits, in the human adult cerebellum and hippocampus. Specimens of human hippocampus and cerebellum were obtained at the time of autopsy from two male individuals, aged 24 and 48 years, with no obvious brain injury. The brains were immunostained using anti-human rabbit polyclonal NR antibodies (NMDA R 2A&B, ΑΒ1548 (Chemicon), NMDA receptors anti-human Poly HRP IHC (Detection kit) and counterstained with Mayer's hematoxylin. The present immunohistochemical research of human adult cerebellum and hippocampus demonstrates that the majority of neurons in the dentate gyrus, the large pyramidal neurons of the hippocampus, the granular cells of the cerebellum as well as the main cerebellar neuron, namely Purkinje cell, stained deeply by the monoclonal antibody, suggesting that the majority of the neuronal network in cerebellum and hippocampus uses as neurotransmitter the excitatory aminoacids on the system of NMDA receptors. Our findings, demonstrating that the majority of cells were stained by the monoclonal antibody, emphasize the importance of the excitatory system of the glutamate and the examined receptors 2A & B, in the human cerebellum and hippocampus in adults, underlying the important role that this system may play in memory function and cognition, and at the same time the crucial role of the cerebellum in higher cognitive functions, in part due to the wide distribution of NMDA R.
    No preview · Dataset · Apr 2013
  • Sochocka M · Koutsouraki E · Gąsiorowski K · Leszek J

    No preview · Dataset · Mar 2013
  • Sochocka M · Koutsouraki E · Gasiorowski K · Leszek J
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    ABSTRACT: Vascular and metabolic dysfunctions and mitochondrial failure are now believed to be contributors to Alzheimer disease (AD) pathogenesis. Vascular dysfunction includes reduced cerebral blood flow (CBF), blood-brain barrier (BBB) disturbances and cerebral amyloid angiopathy (CAA). Mitochondrial failure results in deregulation of Ca2+ homeostasis and elevated reactive oxygen species (ROS) generation, both of which are linked to neurotoxicity. Increased level of ROS stimulates proinflammatory gene transcription and release of cytokines, such as IL-1, IL-6, TNF-α, chemokines thereby induces neuroinflammation. Conversely, inflammatory reactions activate microglia and astrocytes to generation of large amounts of ROS, so neuroinflammation could be perceived as a cause and a consequence of chronic oxidative stress. The interaction between oxidative stress and neuroinflammation leads to amyloid-β (Aβ) generation. The deposition of the Aβ peptide in the brain generates a cascade of pathological events, including the formation of neurofibrillary tangles (NFTs), inflammatory reactions, increased oxidative stress and mitochondrial dysfunction, which are causative factors of cell death and dementia. The purpose of this paper is to provide current evidence on vascular dysfunction and mitochondrial failure, both in neurons, glia and in brain vascular wall-cells in the context of potential application for treatment strategy of AD and other neurodegenerations.
    No preview · Dataset · Mar 2013
  • Sochocka M · Koutsouraki ES · Gąsiorowski K · Leszek J
    [Show abstract] [Hide abstract]
    ABSTRACT: Vascular and metabolic dysfunctions and mitochondrial failure are now believed to be contributors to Alzheimer disease (AD) pathogenesis. Vascular dysfunction includes reduced cerebral blood flow (CBF), blood-brain barrier (BBB) disturbances and cerebral amyloid angiopathy (CAA). Mitochondrial failure results in deregulation of Ca2+ homeostasis and elevated reactive oxygen species (ROS) generation, both of which are linked to neurotoxicity. Increased level of ROS stimulates proinflammatory gene transcription and release of cytokines, such as IL-1, IL-6, TNF-α, chemokines thereby induces neuroinflammation. Conversely, inflammatory reactions activate microglia and astrocytes to generation of large amounts of ROS, so neuroinflammation could be perceived as a cause and a consequence of chronic oxidative stress. The interaction between oxidative stress and neuroinflammation leads to amyloid-β (Aβ) generation. The deposition of the Aβ peptide in the brain generates a cascade of pathological events, including the formation of neurofibrillary tangles (NFTs), inflammatory reactions, increased oxidative stress and mitochondrial dysfunction, which are causative factors of cell death and dementia. The purpose of this paper is to provide current evidence on vascular dysfunction and mitochondrial failure, both in neurons, glia and in brain vascular wall-cells in the context of potential application for treatment strategy of AD and other neurodegenerations.
    No preview · Dataset · Feb 2013
  • Sochocka M · Koutsouraki ES · Gąsiorowski K · Leszek J
    [Show abstract] [Hide abstract]
    ABSTRACT: Vascular and metabolic dysfunctions and mitochondrial failure are now believed to be contributors to Alzheimer disease (AD) pathogenesis. Vascular dysfunction includes reduced cerebral blood flow (CBF), blood-brain barrier (BBB) disturbances and cerebral amyloid angiopathy (CAA). Mitochondrial failure results in deregulation of Ca2+ homeostasis and elevated reactive oxygen species (ROS) generation, both of which are linked to neurotoxicity. Increased level of ROS stimulates proinflammatory gene transcription and release of cytokines, such as IL-1, IL-6, TNF-α, chemokines thereby induces neuroinflammation. Conversely, inflammatory reactions activate microglia and astrocytes to generation of large amounts of ROS, so neuroinflammation could be perceived as a cause and a consequence of chronic oxidative stress. The interaction between oxidative stress and neuroinflammation leads to amyloid-β (Aβ) generation. The deposition of the Aβ peptide in the brain generates a cascade of pathological events, including the formation of neurofibrillary tangles (NFTs), inflammatory reactions, increased oxidative stress and mitochondrial dysfunction, which are causative factors of cell death and dementia. The purpose of this paper is to provide current evidence on vascular dysfunction and mitochondrial failure, both in neurons, glia and in brain vascular wall-cells in the context of potential application for treatment strategy of AD and other neurodegenerations.
    No preview · Dataset · Feb 2013
  • Sochocka M · Koutsouraki ES · Gąsiorowski K · Leszek J
    [Show abstract] [Hide abstract]
    ABSTRACT: Vascular and metabolic dysfunctions and mitochondrial failure are now believed to be contributors to Alzheimer disease (AD) pathogenesis. Vascular dysfunction includes reduced cerebral blood flow (CBF), blood-brain barrier (BBB) disturbances and cerebral amyloid angiopathy (CAA). Mitochondrial failure results in deregulation of Ca2+ homeostasis and elevated reactive oxygen species (ROS) generation, both of which are linked to neurotoxicity. Increased level of ROS stimulates proinflammatory gene transcription and release of cytokines, such as IL-1, IL-6, TNF-α, chemokines thereby induces neuroinflammation. Conversely, inflammatory reactions activate microglia and astrocytes to generation of large amounts of ROS, so neuroinflammation could be perceived as a cause and a consequence of chronic oxidative stress. The interaction between oxidative stress and neuroinflammation leads to amyloid-β (Aβ) generation. The deposition of the Aβ peptide in the brain generates a cascade of pathological events, including the formation of neurofibrillary tangles (NFTs), inflammatory reactions, increased oxidative stress and mitochondrial dysfunction, which are causative factors of cell death and dementia. The purpose of this paper is to provide current evidence on vascular dysfunction and mitochondrial failure, both in neurons, glia and in brain vascular wall-cells in the context of potential application for treatment strategy of AD and other neurodegenerations.
    No preview · Dataset · Feb 2013

  • No preview · Dataset · Oct 2012

  • No preview · Dataset · Oct 2012

  • No preview · Dataset · Oct 2012

  • No preview · Dataset · Oct 2012
  • Source

    Full-text · Article · Sep 2012 · European Journal of Neurology
  • Source
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    ABSTRACT: We examined the sera of 56 patients suffering from definite multiple sclerosis and 60 healthy individuals using ELISA, for investigating the possible connection between IgM antibodies against GM1, GD1b and GQ1b gangliosides and clinical parameters of multiple sclerosis It was revealed no significant comparison between anti-ganglioside antibodies and the grade of disability (based on EDSS), the duration, the types or the therapeutic approach (p>0.05). However there was a positive connection between the EDSS and duration of the disease. Patients with scores in the EDSS scale 4.0-5.5 revealed duration of multiple sclerosis of 14 years (p=0.0005).
    Full-text · Conference Paper · Jun 2012
  • E. Koutsouraki · Th. Kalatha · E. Hatzifilippou · A. Orologas
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    ABSTRACT: Multiple sclerosis (MS) is characterized by inflammatory demyelination and axonal loss as pathophysiological correlates of relapsing activity and progressive development of clinical disability. The molecular processes involved in this pathogenesis are still unclear as they are quite complex and heterogeneous. In the present study we tried to correlate the β-amyloid 42 levels in the cerebrospinal fluid (CSF) of MS patients, using Elisa technique, with clinical parameters and treatment. A total of 20 subjects was evaluated, 13 MS patients (7 Relapsing/Remitting MS, 2 Secondary Progressive MS, 1 Clinical Isolated Syndrome, 1 Progressing/Relapsing MS, 3 Primary Progressive MS) and 7 patients suffered from diseases of the peripheral nervous system, used as controls. The analyzed and statistically evaluated parameters included: CSF β-amyloid 1-42 levels, presence of oligoclonal bands in the CSF, sex, age, type and duration of the disease, Expanded Disability Status Scale values, treatment and co-existence with other diseases. There was no significant correlation between Aβ 42 concentrations and EDSS but the highest values of Aβ 42 were observed in MS patients who suffered from Primary or Secondary progressive type of MS. Our findings are indicative of a probable correlation between CSF Aβ 42 levels and the degeneration occurred during MS.
    No preview · Conference Paper · Jun 2012
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    ABSTRACT: Myasthenia gravis (MG) is an autoimmune disorder of the neuromuscular junction usually caused by antibodies to the nicotinic acetylcholine receptor (AChR) and occasionally to muscle-specific kinase (MuSK). D-penicillamine is a therapeutic agent for several diseases, but can also induce a number of immune-mediated disorders, including MG, as a side-effect. In most patients with D-penicillamine-induced MG, anti-AChR antibodies are detected, but the presence of anti-MuSK antibodies has not been reported previously. The case reported was a female patient who presented with myasthenic symptoms after D-penicillamine administration for scleroderma. Both anti-AChR and anti-MuSK antibodies were identified in the patient's serum. The anti-MuSK antibodies were of the IgG4 subclass, as in idiopathic MG. Both types of antibody gradually disappeared after discontinuation of D-penicillamine. A significant improvement in symptoms was observed and the patient gradually became free of MG symptoms, without requiring any treatment for MG. Another four double-positive (anti-AChR and anti-MuSK antibodies) patients were identified during a retrospective study, but none had been treated with D-penicillamine. D-penicillamine can cause anti-AChR and anti-MuSK antibody-positive MG, a rare phenomenon which is reversed after discontinuation of D-penicillamine treatment.
    Full-text · Article · Jun 2012 · Journal of neuroimmunology

Publication Stats

123 Citations
181.21 Total Impact Points

Institutions

  • 2005-2014
    • Aristotle University of Thessaloniki
      • • Department of Neurology II
      • • Laboratory of Neurophysiology
      Saloníki, Central Macedonia, Greece
  • 2008-2012
    • AHEPA University Hospital
      Saloníki, Central Macedonia, Greece