A5073690506- Alzheimer's disease research and treatments
- Neuroscience and Neuropharmacology Research
- Neuroinflammation and Neurodegeneration Mechanisms
- Anesthesia and Neurotoxicity Research
- Telomeres, Telomerase, and Senescence
- Mitochondrial Function and Pathology
- Olfactory and Sensory Function Studies
- Plant Stress Responses and Tolerance
- Circadian rhythm and melatonin
- Linguistics and Education Research
- Nicotinic Acetylcholine Receptors Study
- Genetics, Aging, and Longevity in Model Organisms
- Vitamin C and Antioxidants Research
- Oral microbiology and periodontitis research
- Anesthesia and Sedative Agents
- Education Pedagogy and Practices
- Cancer-related cognitive impairment studies
- Health and Well-being Studies
- Medicinal Plants and Neuroprotection
- Ion channel regulation and function
- Photochromic and Fluorescence Chemistry
- Biochemical effects in animals
- Biological Research and Disease Studies
- Photoreceptor and optogenetics research
- Nerve injury and regeneration
Hospital de Clínicas
2025
University of Chile
2016-2024
Hospital Clínico de la Universidad de Chile
2021-2023
Increased reactive oxygen species (ROS) generation and the ensuing oxidative stress contribute to Alzheimer’s disease pathology. We reported previously that amyloid- β peptide oligomers (A Os) produce aberrant Ca 2+ signals at sublethal concentrations decrease expression of type-2 ryanodine receptors (RyR2), which are crucial for hippocampal synaptic plasticity memory. Here, we investigated whether antioxidant agent astaxanthin (ATX) protects neurons from A Os-induced excessive mitochondrial...
Aims: Previous studies indicate that hippocampal synaptic plasticity and spatial memory processes entail calcium release from intracellular stores mediated by ryanodine receptor (RyR) channels. In particular, RyR-mediated Ca2+ is central for the dendritic spine remodeling induced brain-derived neurotrophic factor (BDNF), a neurotrophin stimulates complex signaling pathways leading to memory-associated protein synthesis structural plasticity. To examine if upregulation of type-2 (RyR2)...
Introduction: Previous reports have proposed that Periodontal disease (PDis) predisposes to Alzheimer's (AD), both highly prevalent pathologies among the elderly. The bacteria Aggregatibacter actinomycetemcomitans (Aa), associated with most aggressive forms of PDis, are classified in different serotypes distinct virulence according antigenicity their lipopolysaccharide (LPS). Methods: Here, we determined effects purified LPS, from a, b or c Aa, on primary cultures microglia mixed hippocampal...
Abstract Postoperative delirium (POD), an acute cognitive dysfunction linked to morbidity and mortality, is characterized by memory impairments disturbances in consciousness, particularly patients aged 65 older. Neuroinflammation NAD+ imbalance are key mechanisms behind POD, leading synaptic deterioration. However, how surgery contributes POD neuroinflammation remains unclear, effective treatments lacking. Here we used a rodent model of bone fracture examine the impact on plasticity,...
Amyloid β peptide oligomers (AβOs), toxic aggregates with pivotal roles in Alzheimer´s disease, trigger persistent and low magnitude Ca2+ signals neurons. We reported previously that these signals, which arise from entry subsequent amplification by release through ryanodine receptor (RyR) channels, promote mitochondrial network fragmentation reduce RyR2 expression. Here, we examined if AβOs, inducing redox sensitive RyR-mediated release, stimulate Ca2+-uptake, ROS generation fragmentation,...
Recent studies suggest that cellular senescence plays a role in Alzheimer's Disease (AD) pathogenesis. We hypothesize markers might be tracked the peripheral tissues of AD patients. Senescence hallmarks, including altered metabolism, cell-cycle arrest, DNA damage response (DDR) and secretory associated phenotype (SASP), were measured blood mononuclear cells (PBMCs) healthy controls (HC), amnestic mild cognitive impairment (aMCI) Senescence-associated βeta-galactosidase (SA-β-Gal) activity,...
Hippocampal neuronal activity generates dendritic and somatic Ca2+ signals, which depending on stimulus intensity, rapidly propagate to the nucleus induce expression of transcription factors genes with crucial roles in cognitive functions. Soluble Amyloid-beta Oligomers (AβOs), main synaptotoxins engaged pathogenesis Alzheimer's disease, generate aberrant signals primary hippocampal neurons, increase their oxidative tone disrupt structural plasticity. Here, we explored effects...
Hippocampal neuronal activity generates dendritic and somatic Ca2+ signals, which, depending on stimulus intensity, rapidly propagate to the nucleus induce expression of transcription factors genes with crucial roles in cognitive functions. Soluble amyloid-beta oligomers (AβOs), main synaptotoxins engaged pathogenesis Alzheimer's disease, generate aberrant signals primary hippocampal neurons, increase their oxidative tone disrupt structural plasticity. Here, we explored effects sub-lethal...
Abstract Background Predicting Alzheimer's disease (AD) and frontotemporal dementia (FTD) using polygenic risk scores (PRS) for late‐onset forms holds promise, but its accuracy might be influenced by social determinants of health (SDOH). This study explores how considering SDOH alongside genes can improve prediction, focusing on potential differences each disease. Methods Employing logistic regression in 677 individuals (287 AD, 102 FTD, 288 controls) aged 40‐80 from the ReDLat across six...
Abstract Background Most research initiatives have emerged from high‐income countries (HIC), leaving a gap in understanding the disease’s genetic basis diverse populations like those Latin American (LAC). ReDLat tackles this gap, focusing on LAC’s unique genetics and socioeconomic factors to identify specific Alzheimer’s Disease (AD) Frontotemporal Dementia (FTD) risk Mexico, Colombia, Peru, Chile, Argentina, Brazil. Method We employed comprehensive analysis approach, integrating Whole...
Epidemiological studies show that having a history of cancer protects from the development Alzheimer's Disease (AD), and vice versa, AD cancer. The mechanism this mutual protection is unknown. We have reported peripheral blood mononuclear cells (PBMC) amnestic cognitive impairment (aMCI) (AD) patients increased susceptibility to oxidative cell death compared control subjects, opposite standpoint associated with resistance stress in PBMCs, even those subjects who aMCI (Ca + aMCI). Cellular...