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Fernando Juan Pitossi

Researcher at Fundación Instituto Leloir

Publications -  67
Citations -  4869

Fernando Juan Pitossi is an academic researcher from Fundación Instituto Leloir. The author has contributed to research in topics: Substantia nigra & Neurodegeneration. The author has an hindex of 31, co-authored 65 publications receiving 4489 citations. Previous affiliations of Fernando Juan Pitossi include University of Buenos Aires & National Scientific and Technical Research Council.

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Neuronal differentiation in the adult hippocampus recapitulates embryonic development.

TL;DR: It is striking that neuronal maturation in the adult hippocampus follows a precise sequence of connectivity (silent → slow GABA → glutamate → fast GABA) that resembles hippocampal development.
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Transient expression of IL-1beta induces acute lung injury and chronic repair leading to pulmonary fibrosis.

TL;DR: It is shown how acute tissue injury in the lung, initiated by a highly proinflammatory cytokine, IL-1beta, converts to progressive fibrotic changes and should be considered a valid target for therapeutic intervention in diseases associated with fibrosis and tissue remodeling.
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Central and systemic IL-1 exacerbates neurodegeneration and motor symptoms in a model of Parkinson's disease

TL;DR: An unequivocal association between IL-1 overproduction and increased disease progression is demonstrated, pointing to inflammation as a risk factor for Parkinson's disease and suggesting that inflammation should be efficiently handled in patients to slow disease progression.
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BDNF-triggered events in the rat hippocampus are required for both short- and long-term memory formation.

TL;DR: The results indicate that endogenous BDNF is required for both STM and LTM formation of an inhibitory avoidance learning, and suggest that this requirement involves ERK1/2‐dependent and ‐independent mechanisms.
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Neurogenic niche modulation by activated microglia: transforming growth factor β increases neurogenesis in the adult dentate gyrus

TL;DR: This work identified an anti‐inflammatory cytokine, TGF‐β, with neurogenic potential in the adult brain, and supports the idea that activated microglial cells are not pro‐ or anti‐neurogenic per se, but the balance between pro‐ and anti-inflammatory secreted molecules influences the final effect of this activation.