Pedro Cisternas

ORCID: 0000-0001-7796-8982
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About
Contact & Profiles
Research Areas
  • Alzheimer's disease research and treatments
  • Vitamin C and Antioxidants Research
  • Genetics and Neurodevelopmental Disorders
  • Wnt/β-catenin signaling in development and cancer
  • Diet, Metabolism, and Disease
  • Andrographolide Research and Applications
  • Regulation of Appetite and Obesity
  • Liver Disease Diagnosis and Treatment
  • Vitamin D Research Studies
  • Neuroscience and Neuropharmacology Research
  • Biochemical effects in animals
  • Medicinal Plants and Neuroprotection
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Vitamin K Research Studies
  • Electrolyte and hormonal disorders
  • Anesthesia and Neurotoxicity Research
  • Adipose Tissue and Metabolism
  • Cholinesterase and Neurodegenerative Diseases
  • Thyroid Disorders and Treatments
  • Pancreatic function and diabetes
  • Tryptophan and brain disorders
  • Computational Drug Discovery Methods
  • Adipokines, Inflammation, and Metabolic Diseases
  • PARP inhibition in cancer therapy
  • Mitochondrial Function and Pathology

University of O'Higgins
2021-2024

Pontificia Universidad Católica de Chile
2013-2021

Johns Hopkins Medicine
2019

Johns Hopkins University
2019

University of Atacama
2016-2017

University of Concepción
2008-2016

Vitamin C is an essential micronutrient in the human diet; its deficiency leads to a number of symptoms and ultimately death. After entry into cells within central nervous system (CNS) through sodium vitamin transporters (SVCTs) facilitative glucose (GLUTs), functions as neuromodulator, enzymatic cofactor, reactive oxygen species (ROS) scavenger; it also stimulates differentiation. In this review, we will compare molecular structural aspects their expression endothelial or choroid plexus...

10.4172/2157-7633.1000209 article EN Journal of Stem Cell Research & Therapy 2014-01-01

The combination of the scaffolds cholinesterase inhibitor huprine Y and antioxidant capsaicin results in compounds with nanomolar potencies toward human acetylcholinesterase (AChE) butyrylcholinesterase (BChE) that retain or improve properties capsaicin. Crystal structures their complexes AChE BChE revealed molecular basis for high potency. Brain penetration was confirmed by biodistribution studies C57BL6 mice, one compound (5i) displaying better brain/plasma ratio than donepezil. Chronic...

10.1021/acs.jmedchem.0c01775 article EN Journal of Medicinal Chemistry 2020-12-28

Dysregulated Wnt signaling is linked to major neurodegenerative diseases, including Alzheimer disease (AD). In mouse models of AD, activation the canonical pathway improves learning/memory, but mechanism for this remains unclear. The decline in brain function AD patients correlates with reduced glucose utilization by neurons. Here, we test whether improvements metabolism mediate neuroprotective effects model. APPswe/PS1dE9 transgenic mice were used model Andrographolide or Lithium was...

10.1111/jnc.14608 article EN Journal of Neurochemistry 2018-10-10

Abstract Vitamin C is an essential factor for neuronal function and survival, existing in two redox states, ascorbic acid ( AA ), its oxidized form, dehydroascorbic DHA ). Here, we show uptake of both by primary cultures rat brain cortical neurons. Moreover, that most intracellular was rapidly to . Intracellular induced a rapid dramatic decrease reduced glutathione immediately followed spontaneous recovery. This transient oxidation preceded increase the rate glucose through pentose phosphate...

10.1111/jnc.12663 article EN Journal of Neurochemistry 2014-01-25

Ascorbic acid (AA) is best known for its role as an essential nutrient in humans and other species. As the brain does not synthesize AA, high levels are achieved this organ by specific uptake mechanisms, which concentrate AA from bloodstream to CSF intracellular compartment. Two different isoforms of sodium-vitamin C co-transporters (SVCT1 SVCT2) have been cloned. Both SVCT proteins mediate affinity Na(+)-dependent L-AA transport necessary vitamin many tissues. In adult expression SVCT2 was...

10.1111/j.1471-4159.2008.05788.x article EN Journal of Neurochemistry 2008-11-19

Alzheimer's disease (AD) is a neurodegenerative disorder mainly known for synaptic impairment and neuronal cell loss, affecting memory processes. Beside these damages, mitochondria have been implicated in the pathogenesis of AD through induction mitochondrial permeability transition pore (mPTP). The mPTP non-selective that formed under apoptotic conditions, disturbing structure thus, viability. In AD, Aβ oligomers (Aβos) favor opening pore, activating mitochondria-dependent death cascades....

10.1371/journal.pone.0168840 article EN cc-by PLoS ONE 2017-01-06

Alzheimer's disease (AD) is the most common type of dementia. The onset and progression this pathology are correlated with several changes in brain, including formation extracellular aggregates amyloid-beta (Aβ) peptide intracellular accumulation hyperphosphorylated tau protein. In addition, dysregulated neuronal plasticity, synapse loss, a reduction cellular energy metabolism have also been described. Canonical Wnt signaling has shown to be downregulated AD. Remarkably, we showed previously...

10.3389/fncel.2019.00295 article EN cc-by Frontiers in Cellular Neuroscience 2019-07-18

Alzheimer's disease (AD) is the most common neurodegenerative disorder and leading cause of age-related dementia worldwide. Several models for AD have been developed to provide information regarding initial changes that lead degeneration. Transgenic mouse recapitulate many, but not all, features AD, likely because high complexity pathology. In this context, validation a wild-type animal model mimics neuropathological behavioral abnormalities necessary. previous studies, we reported Chilean...

10.1111/bpa.12226 article EN Brain Pathology 2014-10-29

Metabolic syndrome (MetS), a cluster of metabolic conditions that include obesity, hyperlipidemia, and insulin resistance, increases the risk several aging-related brain diseases, including Alzheimer's disease (AD). However, underlying mechanism explaining link between MetS function is poorly understood. Among possible mediators are adipose-derived secreted molecules called adipokines, adiponectin (ApN) resistin, which have been shown to regulate by modulating processes. To investigate...

10.3389/fendo.2023.1237796 article EN cc-by Frontiers in Endocrinology 2023-09-04
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