Search Results - "Kurbatskaya, Ksenia"

Inhibition of glycogen synthase kinase-3 by BTA-EG4 reduces tau abnormalities in an organotypic brain slice culture model of Alzheimer’s disease by Croft, Cara L., Kurbatskaya, Ksenia, Hanger, Diane P., Noble, Wendy

“…Organotypic brain slice culture models provide an alternative to early stage in vivo studies as an integrated tissue system that can recapitulate key disease…”
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A primate-specific short GluN2A-NMDA receptor isoform is expressed in the human brain by Warming, Hannah, Pegasiou, Chrysia-Maria, Pitera, Aleksandra P, Kariis, Hanna, Houghton, Steven D, Kurbatskaya, Ksenia, Ahmed, Aminul, Grundy, Paul, Vajramani, Girish, Bulters, Diederik, Altafaj, Xavier, Deinhardt, Katrin, Vargas-Caballero, Mariana

“…Glutamate receptors of the N-methyl-D-aspartate (NMDA) family are coincident detectors of pre- and postsynaptic activity, allowing Ca influx into neurons…”
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Astrocytes and neuroinflammation in Alzheimer's disease by Phillips, Emma C, Croft, Cara L, Kurbatskaya, Ksenia, O'Neill, Michael J, Hutton, Michael L, Hanger, Diane P, Garwood, Claire J, Noble, Wendy

“…Increased production of amyloid β-peptide (Aβ) and altered processing of tau in Alzheimer's disease (AD) are associated with synaptic dysfunction, neuronal…”
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Upregulation of calpain activity precedes tau phosphorylation and loss of synaptic proteins in Alzheimer's disease brain by Kurbatskaya, Ksenia, Phillips, Emma C, Croft, Cara L, Dentoni, Giacomo, Hughes, Martina M, Wade, Matthew A, Al-Sarraj, Safa, Troakes, Claire, O'Neill, Michael J, Perez-Nievas, Beatriz G, Hanger, Diane P, Noble, Wendy

“…Alterations in calcium homeostasis are widely reported to contribute to synaptic degeneration and neuronal loss in Alzheimer's disease. Elevated cytosolic…”
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Membrane association and release of wild-type and pathological tau from organotypic brain slice cultures by Croft, Cara L, Wade, Matthew A, Kurbatskaya, Ksenia, Mastrandreas, Pavlina, Hughes, Martina M, Phillips, Emma C, Pooler, Amy M, Perkinton, Michael S, Hanger, Diane P, Noble, Wendy

“…The spatiotemporal transmission of pathological tau in the brain is characteristic of Alzheimer’s disease. Release of both soluble and abnormal tau species…”
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Calpain cleavage and inactivation of the sodium calcium exchanger‐3 occur downstream of Aβ in Alzheimer's disease by Atherton, Joe, Kurbatskaya, Ksenia, Bondulich, Marie, Croft, Cara L., Garwood, Claire J., Chhabra, Resham, Wray, Selina, Jeromin, Andreas, Hanger, Diane P., Noble, Wendy

“…Summary Alzheimer's disease (AD) is a neurodegenerative disorder characterized by pathological deposits of β‐amyloid (Aβ) in senile plaques, intracellular…”
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Inhibition of glycogen synthase kinase-3 by BTA-EG 4 reduces tau abnormalities in an organotypic brain slice culture model of Alzheimer's disease by Croft, Cara L, Kurbatskaya, Ksenia, Hanger, Diane P, Noble, Wendy

“…Organotypic brain slice culture models provide an alternative to early stage in vivo studies as an integrated tissue system that can recapitulate key disease…”
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Calcium homeostasis and calciumactivated proteins in alzheimer's disease by Kurbatskaya, Ksenia

“…Ca2+ dyshomeostasis is considered to be an early pathogenic event in Alzheimer’s disease (AD). Abnormal levels and activity of Ca2+-regulated proteins are…”
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Calpain cleavage and inactivation of the sodium calcium exchanger‐3 occur downstream of A β in A lzheimer's disease by Atherton, Joe, Kurbatskaya, Ksenia, Bondulich, Marie, Croft, Cara L., Garwood, Claire J., Chhabra, Resham, Wray, Selina, Jeromin, Andreas, Hanger, Diane P., Noble, Wendy

“…Summary Alzheimer's disease ( AD ) is a neurodegenerative disorder characterized by pathological deposits of β‐amyloid ( A β) in senile plaques, intracellular…”
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Calpain cleavage and inactivation of the sodium calcium exchanger-3 occur downstream of A[beta] in Alzheimer's disease by Atherton, Joe, Kurbatskaya, Ksenia, Bondulich, Marie, Croft, Cara L, Garwood, Claire J, Chhabra, Resham, Wray, Selina, Jeromin, Andreas, Hanger, Diane P, Noble, Wendy

“…Summary Alzheimer's disease (AD) is a neurodegenerative disorder characterized by pathological deposits of [beta]-amyloid (A[beta]) in senile plaques,…”
Get full text