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Christine T. Ekdahl

Researcher at Lund University

Publications -  41
Citations -  5965

Christine T. Ekdahl is an academic researcher from Lund University. The author has contributed to research in topics: Neurogenesis & Hippocampal formation. The author has an hindex of 25, co-authored 39 publications receiving 5581 citations.

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Inflammation is detrimental for neurogenesis in adult brain.

TL;DR: It is demonstrated that lipopolysaccharide-induced inflammation, which gives rise to microglia activation in the area where the new neurons are born, strongly impairs basal hippocampal neurogenesis in rats, raising the possibility that suppression of hippocampal Neurogenesis by activatedmicroglia contributes to cognitive dysfunction in aging, dementia, epilepsy, and other conditions leading to brain inflammation.
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Brain inflammation and adult neurogenesis: the dual role of microglia.

TL;DR: It is concluded that microglia activation, as an indicator of inflammation, is not pro- or antineurogenic per se but the net outcome is dependent on the balance between secreted molecules with pro- and antiinflammatory action.
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Persistent production of neurons from adult brain stem cells during recovery after stroke

TL;DR: It is shown that endogenous neural stem cells continuously supply the injured adult brain with new neurons, which suggests novel self‐repair strategies to improve recovery after stroke.
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Tumor necrosis factor receptor 1 is a negative regulator of progenitor proliferation in adult hippocampal neurogenesis.

TL;DR: In this paper, the TNF-R1 and its receptors play any role for neurogenesis in the adult brain and are found to be a negative regulator of neural progenitor proliferation in both intact and pathological brain.
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Long-term accumulation of microglia with proneurogenic phenotype concomitant with persistent neurogenesis in adult subventricular zone after stroke.

TL;DR: Increased numbers of activated microglia in ipsilateral SVZ concomitant with neuroblast migration into the striatum are demonstrated at 2, 6, and 16 weeks, with maximum at 6 weeks, following 2 h middle cerebral artery occlusion in rats.