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Jerònia Lladó

Researcher at Johns Hopkins University

Publications -  25
Citations -  2844

Jerònia Lladó is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Excitotoxicity & Neuroprotection. The author has an hindex of 20, co-authored 25 publications receiving 2639 citations. Previous affiliations of Jerònia Lladó include University of Seville.

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Retrograde viral delivery of IGF-1 prolongs survival in a mouse ALS model.

TL;DR: It is reported that insulin-like growth factor 1 prolongs life and delays disease progression, even when delivered at the time of overt disease symptoms.
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Tumor necrosis factor alpha: a link between neuroinflammation and excitotoxicity.

TL;DR: This review summarizes the current knowledge of the cellular and molecular mechanisms by which TNF-α links the neuroinflammatory and excitotoxic processes that occur in several neurodegenerative diseases, but with a special emphasis on amyotrophic lateral sclerosis (ALS).
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Human embryonic germ cell derivatives facilitate motor recovery of rats with diffuse motor neuron injury.

TL;DR: It is concluded that cells derived from human pluripotent stem cells have the capacity to restore neurologic function in animals with diffuse motor neuron disease via enhancement of host neuron survival and function.
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Neural stem cells protect against glutamate-induced excitotoxicity and promote survival of injured motor neurons through the secretion of neurotrophic factors

TL;DR: The neuroprotective potential of NSCs was further confirmed in vivo by their ability to protect against motor neuron cell death and it was shown that N SCs can protect spinal cord cultures from experimentally induced excitotoxic damage.
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Vascular endothelial growth factor protects spinal cord motoneurons against glutamate-induced excitotoxicity via phosphatidylinositol 3-kinase.

TL;DR: It is indicated that VEGF has neuroprotective effects in rat spinal cord against chronic glutamate excitotoxicity by activating the PI3‐K/Akt signal transduction pathway and the hypothesis of the potential therapeutic effects of VEGf in the prevention of motoneuron degeneration in human ALS is reinforced.