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Antigoni Ekonomou

Researcher at King's College London

Publications -  22
Citations -  1243

Antigoni Ekonomou is an academic researcher from King's College London. The author has contributed to research in topics: Dentate gyrus & Neurogenesis. The author has an hindex of 16, co-authored 22 publications receiving 1119 citations. Previous affiliations of Antigoni Ekonomou include Imperial College London & University of Patras.

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Endogenous neurogenesis in the human brain following cerebral infarction

TL;DR: The results suggest increased endogenous neurogenesis associated with neovascularization and migration of newly-formed cells towards a region of cerebrovascular damage in the adult human brain and highlight possible mechanisms underlying this process.
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Neurogenic abnormalities in Alzheimer's disease differ between stages of neurogenesis and are partly related to cholinergic pathology

TL;DR: It is concluded that neurogenic abnormalities in AD differ between phases and areas of neurogenesis and stages of AD; while hippocampal stem cells (Musashi-1) decrease, proliferation (nestin) increases and differentiation/migration phase as well as axonal/dendritic targeting (doublecortin and β-III-tubulin) remains virtually unchanged.
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Altered neurogenesis in Alzheimer's disease

TL;DR: A significant reduction of progenitor cells (as labeled by Musashi1) in the SVZ of patients with AD, but an increase in GFAP-negative astrocyte-like cells with progenitors characteristics is indicated.
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Generation of a human embryonic stem cell line encoding the cystic fibrosis mutation ΔF508, using preimplantation genetic diagnosis

TL;DR: A human embryonic stem cell line homozygous for the most common mutation leading to cystic fibrosis in humans (delta F508) has been generated and characterized and presents exciting opportunities to test the efficacy and toxicity of new therapies relevant to CF.
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Neuronal migration and ventral subtype identity in the telencephalon depend on SOX1.

TL;DR: The requirement for SOX1 at a cellular level is addressed, revealing both the nature and timing of the defect and suggesting that other SOXB1 members showing expression in specific neuronal populations are likely to play continuous roles from the establishment of precursors to their final differentiation.