41 documents found, page 1 of 5
Mitochondrial and Redox Changes in Periodontitis and Type 2 Diabetes Human Bloo...
Ferreira, Ildete L.; Costa, Solange; Moraes, Bruno; Costa, Ana; Fokt, Olga; Marinho, Daniela; Alves, Vera; Baptista, Isabel P.; Rego, A. CristinaPeriodontitis (PDT) and type 2 diabetes (T2D) have demonstrated a bidirectional relationship and imbalanced oxidative stress linked to mitochondrial dysfunction. Therefore, we investigated mitochondrial and redox (de)regulation in peripheral blood mononuclear cells (PBMCs) in comorbid T2D-PDT, compared to PDT, T2D patients, and control individuals. PBMCs were analyzed for mitochondrial respiration, reactive oxy...
Extracellular vesicles improve GABAergic transmission in Huntington's disease i...
Beatriz, Margarida; Rodrigues, Ricardo J.; Vilaça, Rita; Egas, Conceição; Pinheiro, Paulo S.; Daley, George Q.; Schlaeger, Thorsten M.; Raimundo, NunoBackground: Extracellular vesicles (EVs) carry bioactive molecules associated with various biological processes, including miRNAs. In both Huntington’s disease (HD) models and human samples, altered expression of miRNAs involved in synapse regulation was reported. Recently, the use of EV cargo to reverse phenotypic alterations in disease models with synaptopathy as the end result of the pathophysiological casca...
Apoe4 and Alzheimer's Disease Pathogenesis-Mitochondrial Deregulation and Targe...
Pires, Mariana; Rego, A. CristinaAPOE ε4 allele (ApoE4) is the primary genetic risk factor for sporadic Alzheimer's disease (AD), expressed in 40-65% of all AD patients. ApoE4 has been associated to many pathological processes possibly linked to cognitive impairment, such as amyloid-β (Aβ) and tau pathologies. However, the exact mechanism underlying ApoE4 impact on AD progression is unclear, while no effective therapies are available for this ...
Mitochondrial Dysfunction and Decreased Cytochrome c in Cell and Animal Models ...
Almeida, Filipa; Ferreira, Ildete L.; Naia, Luana; Marinho, Daniela; Vilaça-Ferreira, Ana Catarina; Costa, Marta D.; Duarte-Silva, SaraMitochondrial dysfunction has been described in many neurodegenerative disorders; however, there is less information regarding mitochondrial deficits in Machado-Joseph disease (MJD), a polyglutamine (polyQ) disorder caused by CAG repeat expansion in the ATXN3 gene. In the present study, we characterized the changes in mitochondrial function and biogenesis markers in two MJD models, CMVMJD135 (MJD135) transgenic...
Uncovering the Early Events Associated with Oligomeric Aβ-Induced Src Activation
Mota, Sandra; Fão, Lígia; Coelho, Patrícia Silva; Rego, A. CristinaSoluble Aβ1-42 oligomers (AβO) are formed in the early stages of Alzheimer's disease (AD) and were previously shown to trigger enhanced Ca2+ levels and mitochondrial dysfunction via the activation of N-methyl-D-aspartate receptors (NMDAR). Src kinase is a ubiquitous redox-sensitive non-receptor tyrosine kinase involved in the regulation of several cellular processes, which was demonstrated to have a reciprocal ...
Reduction of class I histone deacetylases ameliorates ER-mitochondria cross-tal...
Marinho, Daniela; Ferreira, Ildete L.; Lorenzoni, Ricardo; Cardoso, Sandra M.; Santana, Isabel; Rego, A. CristinaSeveral molecular mechanisms have been described in Alzheimer's disease (AD), including repressed gene transcription and mitochondrial and endoplasmic reticulum (ER) dysfunction. In this study, we evaluate the potential efficacy of transcriptional modifications exerted by inhibition or knockdown of class I histone deacetylases (HDACs) in ameliorating ER-mitochondria cross-talk in AD models. Data show increased ...
Simultaneous Alteration of the Circadian Variation of Memory, Hippocampal Synap...
Carvalho da Silva, António M; Lemos, Cristina; Silva, Henrique Bernardo; Ferreira, Ildete L.; Tomé, Ângelo R.; Rego, A. Cristina; Cunha, Rodrigo A.Alzheimer's disease (AD) is characterized by progressive memory deficits accompanied by synaptic and metabolic deficits, namely of mitochondrial function. AD patients also display a disrupted circadian pattern. Thus, we now compared memory performance, synaptic plasticity, and mitochondria function in 24-week-old non-transgenic (non-Tg) and triple transgenic male mice modeling AD (3xTg-AD) at Zeitgeber 04 (ZT-4...
Boldine Attenuates Synaptic Failure and Mitochondrial Deregulation in Cellular ...
Toledo, Juan P.; Fernández-Pérez, Eduardo J.; Ferreira, Ildete L.; Marinho, Daniela; Riffo-Lepe, Nicolas O.; Pineda-Cuevas, Benjamin N.Alzheimer's disease (AD) is the most common cause of senile dementia worldwide, characterized by both cognitive and behavioral deficits. Amyloid beta peptide (Aβ) oligomers (AβO) have been found to be responsible for several pathological mechanisms during the development of AD, including altered cellular homeostasis and synaptic function, inevitably leading to cell death. Such AβO deleterious effects provide a ...
Macroautophagy and Mitophagy in Neurodegenerative Disorders: Focus on Therapeut...
Magalhães, João Duarte; Fão, Lígia; Vilaça, Rita; Cardoso, Sandra Morais; Rego, A. CristinaMacroautophagy, a quality control mechanism, is an evolutionarily conserved pathway of lysosomal degradation of protein aggregates, pathogens, and damaged organelles. As part of its vital homeostatic role, macroautophagy deregulation is associated with various human disorders, including neurodegenerative diseases. There are several lines of evidence that associate protein misfolding and mitochondrial dysfunctio...
Neuronal cell-based high-throughput screen for enhancers of mitochondrial funct...
Naia, Luana Carvalho; Pinho, Catarina M.; Dentoni, Giacomo; Liu, Jianping; Leal, Nuno Santos; Ferreira, Duarte M. S.; Schreiner, BernadetteBackground: Mitochondrial dysfunction is a common feature of aging, neurodegeneration, and metabolic diseases. Hence, mitotherapeutics may be valuable disease modifiers for a large number of conditions. In this study, we have set up a large-scale screening platform for mitochondrial-based modulators with promising therapeutic potential. Results: Using differentiated human neuroblastoma cells, we screened 1200 F...