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Paula I. Moreira

Researcher at University of Coimbra

Publications -  280
Citations -  31570

Paula I. Moreira is an academic researcher from University of Coimbra. The author has contributed to research in topics: Oxidative stress & Mitochondrion. The author has an hindex of 70, co-authored 268 publications receiving 26670 citations. Previous affiliations of Paula I. Moreira include Case Western Reserve University & University of Texas at San Antonio.

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Oxidative stress mechanisms and potential therapeutics in Alzheimer disease

TL;DR: The clarification of these phenomena can open a new window for understanding the mechanisms underlying neurodegeneration and, consequently, for the development of new therapeutic strategies such as gene therapy and new pharmaceutical formulations with antioxidant and chelating properties.
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Physical exercise as a possible strategy for brain protection: Evidence from mitochondrial-mediated mechanisms

TL;DR: The present review aims to discuss the role of physical exercise in the modulation of the mechanisms involved in neuroprotection including the activation of signaling pathways underlying brain protection.
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Mitochondrial abnormalities in a streptozotocin-induced rat model of sporadic Alzheimer's disease.

TL;DR: The results demonstrate that the insulin-resistant brain state that characterizes this rat model of sAD is accompanied by the occurrence of mitochondrial abnormalities reinforcing the validity of this animal model to study sAD pathogenesis and potential therapies.
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Metformin protects the brain against the oxidative imbalance promoted by type 2 diabetes.

TL;DR: Results indicate that met formin protects against diabetes-associated oxidative stress suggesting that metformin could be an effective neuroprotective agent.
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Cardiolipin profile changes are associated to the early synaptic mitochondrial dysfunction in Alzheimer's disease.

TL;DR: In contrast to synaptic mitochondria, results support the idea that non-synaptic mitochondria function is preserved at the age of 3 months, and connect specific lipidomic changes with synaptic bioenergetic deficit that may contribute to the progressive synapses loss and the neurodegenerative process that characterizes AD.