Paula I. Moreira
University of Coimbra
283 Papers
1.5K Citations
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. Previous affiliations of Paula I. Moreira include Case Western Reserve University & University of Texas at San Antonio.
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Papers
Cortical and hippocampal mitochondria bioenergetics and oxidative status during hyperglycemia and/or insulin-induced hypoglycemia.
TL;DR: The results suggest that the poor glycemic control that occurs in type 1 diabetic patients undergoing insulin therapy may have detrimental effects in brain areas involved in learning and memory.
Mitochondria, endoplasmic reticulum and innate immune dysfunction in mood disorders: Do Mitochondria-Associated Membranes (MAMs) play a role?
Rosa Resende,Tânia Fernandes,Ana Catarina Pereira,J. De Pascale,Ana Patrícia Marques,Pedro Oliveira,Sofia Morais,Vítor Santos,Nuno Madeira,Cláudia Pereira,Paula I. Moreira +10 more
TL;DR: Current understanding of the role of mitochondria and ER dysfunction under pathological brain conditions particularly in major depressive disorder (MDD) and BD that support the hypothesis that MAMs can act in these mood disorders as the link connecting ER-related stress response and mitochondrial impairment are outlined.
Nucleic acid oxidation in Alzheimer disease.
Paula I. Moreira,Akihiko Nunomura,Masao Nakamura,Atsushi Takeda,Justin C. Shenk,Gjumrakch Aliev,Mark A. Smith,George Perry,George Perry +8 more
TL;DR: Data is presented supporting the notion that mitochondrial and metal abnormalities are key sources of oxidative stress in Alzheimer disease and the mechanisms of nucleic acid oxidation and repair are outlined.
Uncoupling Protein 2 Inhibition Exacerbates Glucose Fluctuation-Mediated Neuronal Effects
TL;DR: Observations suggest that UCP2 is in the core of neuronal cell protection and/or adaptation against GV-mediated effects and that other isoforms of neuronal UCPs can be upregulated to compensate the inhibition of U CP2 activity.
Oxidative stress: the old enemy in Alzheimer's disease pathophysiology.
Paula I. Moreira,Kazuhiro Honda,Quan Liu,Maria S. Santos,Catarina R. Oliveira,Gjumrakch Aliev,Akihiko Nunomura,Xiongwei Zhu,Mark A. Smith,George Perry +9 more
TL;DR: During the progression of the disease, the antioxidant activity of both agents evolves into pro-oxidant activity representing a typical gain-of-function transformation, which can result from an increase in reactive species and a decrease in clearance mechanisms.