Search

Your search keyword '"Sargiannidou, Irene"' showing total 170 results
Start Over Author "Sargiannidou, Irene"
170 results on '"Sargiannidou, Irene"'

3. Glial Cells as Key Regulators in Neuroinflammatory Mechanisms Associated with Multiple Sclerosis.

Author

Theophanous, Styliani, Sargiannidou, Irene, and Kleopa, Kleopas A.

Subjects
*NEUROGLIA, *CELL communication, *MICROGLIA, *DISEASE progression, *COMMUNICATION barriers, *OLIGODENDROGLIA
Abstract

Even though several highly effective treatments have been developed for multiple sclerosis (MS), the underlying pathological mechanisms and drivers of the disease have not been fully elucidated. In recent years, there has been a growing interest in studying neuroinflammation in the context of glial cell involvement as there is increasing evidence of their central role in disease progression. Although glial cell communication and proper function underlies brain homeostasis and maintenance, their multiple effects in an MS brain remain complex and controversial. In this review, we aim to provide an overview of the contribution of glial cells, oligodendrocytes, astrocytes, and microglia in the pathology of MS during both the activation and orchestration of inflammatory mechanisms, as well as of their synergistic effects during the repair and restoration of function. Additionally, we discuss how the understanding of glial cell involvement in MS may provide new therapeutic targets either to limit disease progression or to facilitate repair. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

11. Preliminary In Vitro and In Vivo Insights of In Silico Candidate Repurposed Drugs for Alzheimer's Disease.

Author

Savva, Kyriaki, Zachariou, Margarita, Kynigopoulos, Demos, Fella, Eleni, Vitali, Maria-Ioanna, Kosofidou, Xeni, Spyrou, Michail, Sargiannidou, Irene, Panayiotou, Elena, Dietis, Nikolas, and Spyrou, George M.

Subjects
ALZHEIMER'S disease, ENZYME-linked immunosorbent assay, NEURODEGENERATION, DONEPEZIL, THERAPEUTICS, DRUGS, NEUROFIBRILLARY tangles, CLOMIPHENE
Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disease and is the most common type of dementia. Although a considerably large amount of money has been invested in drug development for AD, no disease modifying treatment has been detected so far. In our previous work, we developed a computational method to highlight stage-specific candidate repurposed drugs against AD. In this study, we tested the effect of the top 13 candidate repurposed drugs that we proposed in our previous work in a severity stage-specific manner using an in vitro BACE1 assay and the effect of a top-ranked drug from the list of our previous work, tetrabenazine (TBZ), in the 5XFAD as an AD mouse model. From our in vitro screening, we detected 2 compounds (clomiphene citrate and Pik-90) that showed statistically significant inhibition against the activity of the BACE1 enzyme. The administration of TBZ at the selected dose and therapeutic regimen in 5XFAD in male and female mice showed no significant effect in behavioral tests using the Y-maze and the ELISA immunoassay of Aβ40. To our knowledge, this is the first time the drug tetrabenazine has been tested in the 5XFAD mouse model of AD in a sex-stratified manner. Our results highlight 2 drugs (clomiphene citrate and Pik-90) from our previous computational work for further investigation. [ABSTRACT FROM AUTHOR]

Published
2023
Full Text
View/download PDF

34. Gene replacement therapy in a model of Charcot-Marie-Tooth 4C neuropathy

Author

Schiza, Natasa, primary, Georgiou, Elena, additional, Kagiava, Alexia, additional, Médard, Jean-Jacques, additional, Richter, Jan, additional, Tryfonos, Christina, additional, Sargiannidou, Irene, additional, Heslegrave, Amanda J, additional, Rossor, Alexander M, additional, Zetterberg, Henrik, additional, Reilly, Mary M, additional, Christodoulou, Christina, additional, Chrast, Roman, additional, and Kleopa, Kleopas A, additional

Published
2019
Full Text
View/download PDF

40. Axonal Pathology Precedes Demyelination in a Mouse Model of X-Linked Demyelinating/ Type I Charcot-Marie Tooth (CMT1X) Neuropathy

Author

Vavlitou, Natalie, Sargiannidou, Irene, Markoullis, Kyriaki, Kyriacou, Kyriacos, Scherer, Steven S., and Kleopa, Kleopas A.

Subjects
Mice, Knockout, Amyloid beta-Protein Precursor, Disease Models, Animal, Mice, nervous system, Charcot-Marie-Tooth Disease, Cell Adhesion Molecules, Neuronal, Nerve Degeneration, Animals, Article, Axons, Connexins, Demyelinating Diseases
Abstract

The X-linked demyelinating/type I Charcot-Marie-Tooth neuropathy (CMT1X) is an inherited peripheral neuropathy caused by mutations in GJB1, the gene that encodes the gap junction protein connexin32. Connexin32 is expressed by myelinating Schwann cells and forms gap junctions in noncompact myelin areas, but axonal involvement is more prominent in X-linked compared with other forms of demyelinating Charcot-Marie-Tooth disease. To clarify the cellular and molecular mechanisms of axonal pathology in CMT1X, we studied Gjb1-null mice at early stages (i.e. 2-4 months old) of the neuropathy, when there is minimal or no demyelination. The diameters of large myelinated axons were progressively reduced in Gjb1-null mice compared with those in wild-type littermates. Furthermore, neurofilaments were relatively more dephosphorylated and more densely packed starting at 2 months of age. Increased expression of β-amyloid precursor protein, a marker of axonal damage, was also detected in Gjb1-null nerves. Finally, fast axonal transport, assayed by sciatic nerve ligation experiments, was slower in distal axons of Gjb1-null versus wild-type animals with reduced accumulation of synaptic vesicle-associated proteins. These findings demonstrate that axonal abnormalities including impaired cytoskeletal organization and defects in axonal transport precede demyelination in this mouse model of CMT1X.

Published
2010

48. The Functional Significance of the CSVTCG-Specific Receptor in Breast Carcinoma Progression

Author

HAHNEMANN UNIV PHILADELPHIA PA, Sargiannidou, Irene, Tuszynski, George, HAHNEMANN UNIV PHILADELPHIA PA, Sargiannidou, Irene, and Tuszynski, George

Abstract

We have isolated a novel CSVTCG-specific tumor cell adhesion receptor and shown by immunohistochemical staining of human breast tumors that the receptor localizes to malignant ductal epithelium while no staining of epithelium in normal and benign tissues was observed. Preliminary studies suggest that the CSVTCO-specific receptor may function to promote the invasive behavior of breast epithelium and contribute to the development of malignancy. To test this hypothesis, we proposed to transfer full-length receptor cDNA in the sense or antisense orientation in order to either over-express or block receptor expression in breast carcinoma cell lines. After successful cloning of the receptor cDNA, clones were selected and evaluated for the expression level of the receptor. Stably transfected cell lines would then be evaluated for their in vitro cell invasive activities as well as their capacity to metastasize and form tumors in vitro and in athymic mice. These studies should provide information on the role of the CSVTCG-specific receptor in breast cancer progression and identify a new target for the development of anti-tumor therapeutics., Original contains color plates: All DTIC reproductions will be in black and white.

Published
2002

49. The Functional Significance of the CSVTCG-Specific Receptor in Breast Carcinoma Progression

Author

HAHNEMANN UNIV PHILADELPHIA PA, Sargiannidou, Irene, Tuszynski, George, HAHNEMANN UNIV PHILADELPHIA PA, Sargiannidou, Irene, and Tuszynski, George

Abstract

We have isolated a novel CSVTCG-specific tumor cell adhesion receptor and shown by immunohistochemical staining of human breast tumors that the receptor localizes to malignant ductal epithelium while no staining of epithelium in normal and benign tissues was observed. Preliminary studies suggest that the CSVTCG-specific receptor may function to promote the invasive behavior of breast epithelium and contribute to the development of malignancy. To test this hypothesis, we propose to transfect tall-length receptor cDNA in the sense or antisense orientation in order to either over-express or block receptor expression in breast carcinoma cell lines. We will use vector constructs that constitutively express the green fluorescent protein in order to enable localization of tumor cells in our animal studies.

Published
2001

Catalog

Books, media, physical & digital resources
See catalog results