Chiara Burgaletto

ORCID: 0000-0002-5517-8223
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About
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Research Areas
  • Alzheimer's disease research and treatments
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Tryptophan and brain disorders
  • Cell death mechanisms and regulation
  • Immune Response and Inflammation
  • Trace Elements in Health
  • Cholinesterase and Neurodegenerative Diseases
  • Nicotinic Acetylcholine Receptors Study
  • Parkinson's Disease Mechanisms and Treatments
  • Chronic Lymphocytic Leukemia Research
  • Inflammation biomarkers and pathways
  • Cancer Immunotherapy and Biomarkers
  • Advanced Breast Cancer Therapies
  • COVID-19 and healthcare impacts
  • COVID-19 Clinical Research Studies
  • Diabetes Treatment and Management
  • Receptor Mechanisms and Signaling
  • Immune cells in cancer
  • Lipid Membrane Structure and Behavior
  • Biochemical Analysis and Sensing Techniques
  • Metabolism, Diabetes, and Cancer
  • Nerve injury and regeneration
  • Chronic Myeloid Leukemia Treatments
  • Pharmacology and Obesity Treatment
  • Ocular Surface and Contact Lens

University of Catania
2018-2025

Weizmann Institute of Science
2021-2025

Alzheimer's disease (AD) is a neurodegenerative disorder that progressively compromises cognitive functions. Tumor necrosis factor (TNF)-Related Apoptosis Inducing Ligand (TRAIL), proinflammatory cytokine belonging to the TNF superfamily, appears be key player in inflammatory/immune orchestra of AD brain. Despite ability an anti-TRAIL monoclonal antibody reach brain producing beneficial effects mice, we attempted develop such TRAIL-neutralizing adsorbed on lipid and polymeric nanocarriers,...

10.3390/biomedicines10050985 article EN cc-by Biomedicines 2022-04-23

Introduction: Alzheimer’s disease (AD) is the most common neurodegenerative disorder affecting elderly population worldwide. Due to multifactorial nature of disease, involving impairment cholinergic neurotransmission and immune system, previous attempts find effective treatments have faced challenges. Methods: In such scenario, we attempted investigate effects alpha-glyceryl-phosphoryl-choline (α-GPC), a cholinomimetic molecule, on neuroinflammation memory outcome in triple transgenic mouse...

10.3389/fphar.2024.1386224 article EN cc-by Frontiers in Pharmacology 2024-03-26

Currently, there are no effective therapeutic options for Alzheimer's disease, the most common, multifactorial form of dementia, characterized by anomalous amyloid accumulation in brain. Growing evidence points to neuroinflammation as a major promoter AD. We have previously shown that proinflammatory cytokine TNFSF10 fuels AD neuroinflammation, and its immunoneutralization results improved cognition 3xTg-AD mouse. Here, we hypothesize inflammatory hallmarks might parallel with central...

10.1186/s12974-019-1554-9 article EN cc-by Journal of Neuroinflammation 2019-08-13

Abstract Age-related disorders, such as Alzheimer’s disease (AD) and age-related macular degeneration (AMD) share common features amyloid-β (Aβ) protein accumulation. Retinal deposition of Aβ aggregates in AMD patients has suggested a potential link between AD. In the present study, we analyzed expression pattern focused set miRNAs, previously found to be involved both AD AMD, retina triple transgenic mouse model (3xTg-AD) at different time-points. Several miRNAs were differentially...

10.1038/s41419-021-04165-x article EN cc-by Cell Death and Disease 2021-10-05

Alzheimer’s disease (AD), marked by cognitive impairment, predominantly affects the brain regions regulated cholinergic innervation, such as cerebral cortex and hippocampus. Cholinergic dysfunction, a key contributor to age-related decline, has spurred investigations into potential therapeutic interventions. We have previously shown that choline alphoscerate (α-GPC), neurotransmission-enhancing agent, protects from Aβ-mediated neurotoxicity. Herein, we investigated effects of α-GPC on...

10.3390/cells13040309 article EN cc-by Cells 2024-02-07

Alzheimer's disease (AD) is the most common cause of dementia worldwide, characterized by accumulation amyloid-β protein and hyperphosphorylated tau in brain. Neuroinflammation, resulting from chronic activation brain-resident innate immune cells as well enhanced peripheral leukocyte access across blood-brain barrier, crucially affects AD progression. In this context, TNFSF10, a cytokine substantially expressed brain, has been shown to modulate both adaptive branches response AD-related...

10.1007/s11481-025-10177-7 article EN cc-by Journal of Neuroimmune Pharmacology 2025-02-07

To investigate the ocular pharmacological profile of hydrocortisone (HC) using in vitro and vivo models dry eye disease. Rabbit corneal epithelial cells (SIRCs) were used to assess effect HC two paradigms damage: hyperosmotic stress scratch-wound assay. Dry was induced albino rabbits by topical administration atropine sulfate or injection concanavalin A (ConA) into lacrimal gland. TNFα, TNF-related apoptosis-inducing ligand (TRAIL), IL-1β, IL-8 determined ELISA western blot a damage model,...

10.3389/fphar.2019.01240 article EN cc-by Frontiers in Pharmacology 2019-10-18

Currently 1.3 billion individuals globally engage in smoking, leading to significant morbidity and mortality, particularly among diabetic patients. There is urgent need for a better understanding of how smoking influences antidiabetic treatment efficacy. The review underscores the role cigarette smoke, polycyclic aromatic hydrocarbons (PAHs), modulating metabolic pathways drugs, primarily through induction cytochrome P450 (CYP450) enzymes uridine diphosphate (UDP)-glucuronosyltransferases...

10.3389/fphar.2024.1406860 article EN cc-by Frontiers in Pharmacology 2024-06-18

Marketed drugs for Parkinson's disease (PD) treat motor symptoms but are ineffective in stopping or slowing progression. In the quest of novel pharmacological approaches that may target progression, drug-repurposing provides a strategy to accelerate preclinical and clinical testing already approved other medical indications. Here, we targeted inflammatory component PD pathology, by first time disease-modifying properties immunomodulatory imide drug (IMiD) pomalidomide translational rat model...

10.1007/s13311-022-01182-2 article EN cc-by Neurotherapeutics 2022-01-01

TRAIL, a member of TNF superfamily, is potent inducer neuronal death. Neurotoxic effects TRAIL appear mediated by its death receptor TRAIL-R2/DR5. To assess the role TRAIL/TRAIL-R2 pathway in AD-related neurodegeneration, we studied impact treatment with amyloid-β (Aβ) upon cell viability and inflammation TRAIL-R-deficient mice (TRAIL-R−/−). Here, demonstrate that lack TRAIL-R2 protects from cultured TRAIL-R−/− mouse embryonic hippocampal cells after either Aβ1-42 or TRAIL. Consistently,...

10.3390/ijms231911625 article EN International Journal of Molecular Sciences 2022-10-01

Since the start of global spread coronavirus disease (COVID-19) pandemic, cancer patients were identified as a specifically susceptible subgroup patient population. Several reports have shown that an increased risk both contracting infection and experiencing more severe course, with rapidly evolving picture associated higher mortality. The assumption “COVID-19 vulnerable” has led, irretrievably, to profound changes in decision making oncological treatments. Potential justifications for such...

10.3390/cancers13081906 article EN Cancers 2021-04-15

Alzheimer's disease (AD) is the most common form of neurodegenerative disorder characterized by cognitive impairment, which represents an urgent public health concern. Given worldwide impact AD, there a compelling need for effective therapies to slow down or halt this disorder.Choline alphoscerate (α-GPC) potentially cholinergic neurotransmission enhancing agent with interesting clinical profile in dysfunctions improvement, although only scanty data are available about mechanisms underlying...

10.2174/1567205018666210608093658 article EN Current Alzheimer Research 2021-04-01

Tumor necrosis factor‐related apoptosis‐inducing ligand ( TRAIL ), a cytokine belonging to the TNF superfamily, is regarded as mediator of neurotoxicity. The constitutively expressed ion exchanger Na + /Ca 2+ isoform‐3 NCX 3) has been shown protect neurons from injury. Its expression induced by nerve growth factor NGF ) through activation its tyrosine kinase receptor trkA. latter, in turn, activates downstream kinases, such extracellular signal‐regulated ERK and survival‐related protein B...

10.1111/febs.14732 article EN FEBS Journal 2018-12-15

OPINION article Front. Oncol., 21 July 2020Sec. Cancer Epidemiology and Prevention Volume 10 - 2020 | https://doi.org/10.3389/fonc.2020.01340

10.3389/fonc.2020.01340 article EN cc-by Frontiers in Oncology 2020-07-21

Parkinson's disease displays clinical heterogeneity, presenting with motor and non-motor symptoms. Heterogeneous phenotypes, named brain-first body-first, may reflect distinct α-synuclein pathology starting either in the central nervous system or periphery. The immune plays a prominent role peripheral pathology, misfolded being placed at intersection between neurodegeneration inflammation. Here, we characterized inflammatory profile immune-phenotype of blood mononuclear cells (PBMCs) from...

10.1007/s00415-024-12554-3 article EN cc-by Journal of Neurology 2024-07-10

Abstract TRAIL, a member of TNF superfamily, is potent inducer neuronal death. Neurotoxic effects TRAIL appear mediated by its death receptor TRAIL-R2/DR5. To assess the role TRAIL/TRAIL-R2 pathway in AD-related neurodegeneration, we studied impact treatment with amyloid-β (Aβ) upon cell viability and inflammation TRAIL-R-deficient mice (TRAIL-R -/- ). Here, demonstrate that lack TRAIL-R2 protects from cultured TRAIL-R mouse embryonic hippocampal cells undergone either Aβ1–42 or TRAIL....

10.21203/rs.3.rs-1124682/v2 preprint EN cc-by Research Square (Research Square) 2022-08-08

Abstract TRAIL, a member of TNF superfamily, is potent inducer neuronal death. Neurotoxic effects TRAIL appear mediated by its death receptor TRAIL-R2/DR5. To assess the role TRAIL/TRAIL-R2 pathway in AD-related neurodegeneration, we studied impact treatment with amyloid-β (Aβ) upon cell viability and inflammation TRAIL-R-deficient mice (TRAIL-R -/- ). Here, demonstrate that lack TRAIL-R2 protects from cultured TRAIL-R mouse embryonic hippocampal cells undergone either Aβ1-42 or TRAIL....

10.21203/rs.3.rs-1124682/v1 preprint EN cc-by Research Square (Research Square) 2021-12-08
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