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
Autophagy in Alzheimer's disease.
Paula I. Moreira,Renato X. Santos,Xiongwei Zhu,Hyoung Gon Lee,Mark A. Smith,Gemma Casadesus,George Perry +6 more
TL;DR: Understanding the exact role of autophagy in different stages of AD progression may help to design more effective therapeutic strategies, and why and when responses to stress or injury can help prevent neuronal degeneration and death.
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High-sugar Diets, Type 2 Diabetes and Alzheimer's Disease
TL;DR: Dietary changes can significantly reduce the risk of T2D and Alzheimer's disease and thereby increase the quality of life and improve longevity.
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Diminished O-GlcNAcylation in Alzheimer's disease is strongly correlated with mitochondrial anomalies
TL;DR: Results suggest that O-GlcNAcylation is involved in AD pathology functioning as a potential link between mitochondrial energetic crisis and synaptic and neuronal degeneration and represents a promising therapeutic target to tackle this devastating neurodegenerative disease.
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Alzheimer's disease-related misfolded proteins and dysfunctional organelles on autophagy menu.
TL;DR: An overview on the role of autophagy on Aβ metabolism, tau processing and clearance, and the contribution of ER-phagy and mitophagy to AD pathology is provided.
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Amyloid-Beta Disrupts Calcium and Redox Homeostasis in Brain Endothelial Cells
Ana Catarina R.G. Fonseca,Paula I. Moreira,Catarina R. Oliveira,Sandra M. Cardoso,Paolo Pinton,Cláudia Pereira +5 more
TL;DR: Using rat brain microvascular endothelial cells, it is found that short-term treatment with a toxic dose of Aβ1-40 inhibits the Ca2+ refill and retention ability of the endoplasmic reticulum and enhances the mitochondrial and cytosolic response to adenosine triphosphate (ATP)-stimulated endoplasmsic Reticulum Ca2- release.
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