Luca Steardo

ORCID: 0000-0003-3570-2195
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Tryptophan and brain disorders
  • Stress Responses and Cortisol
  • Neurotransmitter Receptor Influence on Behavior
  • Cannabis and Cannabinoid Research
  • Receptor Mechanisms and Signaling
  • Neuropeptides and Animal Physiology
  • Neuroendocrine regulation and behavior
  • Migraine and Headache Studies
  • Alzheimer's disease research and treatments
  • Diet and metabolism studies
  • Regulation of Appetite and Obesity
  • Circadian rhythm and melatonin
  • Growth Hormone and Insulin-like Growth Factors
  • Pharmacological Receptor Mechanisms and Effects
  • Eating Disorders and Behaviors
  • Electrolyte and hormonal disorders
  • S100 Proteins and Annexins
  • Pharmacological Effects and Toxicity Studies
  • Neuroscience of respiration and sleep
  • Pituitary Gland Disorders and Treatments
  • Adipose Tissue and Metabolism
  • Immune Response and Inflammation
  • Biochemical effects in animals
  • Cholinesterase and Neurodegenerative Diseases

Sapienza University of Rome
2008-2021

Giustino Fortunato University
2020-2021

University of Naples Federico II
1985-2018

Azienda Ospedaliero-Universitaria Policlinico - Vittorio Emanuele
2007

University of Campania "Luigi Vanvitelli"
1995-2007

University of Palermo
2000-2005

University of Bari Aldo Moro
1993-2004

Federico II University Hospital
1983-1996

University of Chieti-Pescara
1996

Royal Hallamshire Hospital
1996

Peroxisome proliferator-activated receptor-γ (PPARγ) has been reported to be involved in the etiology of pathological features Alzheimer's disease (AD). Cannabidiol (CBD), a Cannabis derivative devoid psychomimetic effects, attracted much attention because its promising neuroprotective properties rat AD models, even though mechanism responsible for such actions remains unknown. This study was aimed at exploring whether CBD effects could subordinate activity PPARγ, which recently indicated as...

10.1371/journal.pone.0028668 article EN cc-by PLoS ONE 2011-12-05

<h3>Objective</h3> Enteric glia activation has been reported to amplify intestinal inflammation via the enteroglial-specific S100B protein. This neurotrophin promotes macrophage recruitment in mucosa, colonic and interacts with toll-like receptors (TLR). Molecules inhibiting S100B-driven enteric might mitigate course of ulcerative colitis (UC). study aims investigate effects palmitoylethanolammide (PEA), a drug able counteract astroglial central nervous system, on inflammation, humans mice....

10.1136/gutjnl-2013-305005 article EN Gut 2013-09-30

Pharmacological inhibition of beta-amyloid (Abeta) induced reactive gliosis may represent a novel rationale to develop drugs able blunt neuronal damage and slow the course Alzheimer's disease (AD). Cannabidiol (CBD), main non-psychotropic natural cannabinoid, exerts in vitro combination neuroprotective effects different models Abeta neurotoxicity. The present study, performed mouse model AD-related neuroinflammation, was aimed at confirming vivo previously reported antiinflammatory...

10.1038/sj.bjp.0707337 article EN British Journal of Pharmacology 2007-06-25

Dieting to control body weight involves cycles of deprivation from palatable food that can promote compulsive eating. The present study shows rats withdrawn intermittent access exhibit overeating upon renewed and an affective withdrawal-like state characterized by corticotropin-releasing factor-1 (CRF(1)) receptor antagonist-reversible behaviors, including hypophagia, motivational deficits obtain less food, anxiogenic-like behavior. Withdrawal was accompanied increased CRF expression CRF(1)...

10.1073/pnas.0908789106 article EN Proceedings of the National Academy of Sciences 2009-11-10

Enteric glial cells (EGC) actively mediate acute and chronic inflammation in the gut; EGC proliferate release neurotrophins, growth factors, pro-inflammatory cytokines which, turn, may amplify immune response, representing a very important link between nervous systems intestine. Cannabidiol (CBD) is an interesting compound because of its ability to control reactive gliosis CNS, without any unwanted psychotropic effects. Therefore rationale our study was investigate effect CBD on intestinal...

10.1371/journal.pone.0028159 article EN cc-by PLoS ONE 2011-12-06

Little is known about the pathophysiology of cerebral edema and other disturbances water balance that involve barrier tissues at interface blood brain. The present experiments show these contain receptors second messenger systems for atriopeptins, recently identified cardiac peptides involved in peripheral regulation. They also atriopeptins can alter rate cerebrospinal fluid production. Because blood-brain blood-cerebrospinal barriers are normal movements central nervous system, studies...

10.1126/science.2879355 article EN Science 1987-01-23

Astroglia are the homoeostatic cells of central nervous system that control a normal function synaptically connected neuronal networks and contribute to brain defense. Recent advances in comprehension pathological potential astroglia indicate astrocytes fundamental for most (if not all) neurological diseases. Neuropathological neuroimaging studies demonstrate prominent astroglial atrophy asthenia occurring neuropsychiatric illnesses. In chronic diseases such as schizophrenia major...

10.1177/1073858413510208 article EN The Neuroscientist 2013-12-03

The aim of this study was to investigate whether prenatal exposure the cannabinoid CB1 receptor agonist WIN 55,212-2 (WIN) at a daily dose devoid overt signs toxicity and/or gross malformations (0.5 mg/kg, gestation days 5-20), influences cortical glutamatergic neurotransmission, learning and emotional reactivity in rat offspring. Basal K+-evoked extracellular glutamate levels were significantly lower cell cultures obtained from pups exposed during with respect those measured neonates born...

10.1093/cercor/bhi076 article EN Cerebral Cortex 2005-03-23

In the central nervous system glial-derived S100B protein has been associated with inflammation via nitric oxide (NO) production. As role of enteroglial cells in inflammatory bowel disease poorly investigated humans, we evaluated association and NO production ulcerative colitis (UC). mRNA expression, inducible synthase (iNOS) were rectal biopsies from 30 controls 35 UC patients. To verify correlation between production, exposed to S100B, presence or absence specific receptor for advanced...

10.1111/j.1365-2982.2009.01346.x article EN Neurogastroenterology & Motility 2009-06-24

Down syndrome (DS) is caused by trisomy of chromosome 21 and characterized mental retardation, seizures premature Alzheimer's disease. To examine neuropathological mechanisms giving rise to this disorder, we generated multiple human DS neural progenitor cell (NPC) lines from the 19–21 week frontal cortex their genomic functional properties. Microarray profiling progenitors indicated that increased levels gene expression were not limited 21, suggesting genes on altered transcriptional...

10.1093/hmg/ddm322 article EN Human Molecular Genetics 2007-11-05

Abstract Background In addition to cytotoxic mechanisms directly impacting neurons, β-amyloid (Aβ)-induced glial activation also promotes release of proinflammatory molecules that may self-perpetuate reactive gliosis and damage neighbouring thus amplifying neuropathological lesions occurring in Alzheimer's disease (AD). Palmitoylethanolamide (PEA) has been studied extensively for its anti-inflammatory, analgesic, antiepileptic neuroprotective effects. PEA is a lipid messenger isolated from...

10.1186/1742-2094-9-49 article EN cc-by Journal of Neuroinflammation 2012-03-09

Emerging evidence indicates that astrogliosis is involved in the pathogenesis of neurodegenerative disorders. Our previous findings suggested cannabinoids and Autacoid Local Injury Antagonism Amides (ALIAmides) attenuate glial response models neurodegeneration. The present study was aimed at exploring palmitoylethanolamide (PEA) ability to mitigate β-amyloid (Aβ)-induced astrogliosis. Experiments were carried out investigate PEA's (10(-7) M) effects upon expression release pro-inflammatory...

10.1111/j.1582-4934.2011.01267.x article EN other-oa Journal of Cellular and Molecular Medicine 2011-01-21

Down syndrome (DS) is a developmental disorder associated with mental retardation (MR) and early onset Alzheimer's disease (AD). These CNS phenotypes are attributed to ongoing neuronal degeneration due constitutive overexpression of chromosome 21 (HSA21) genes. We have previously shown that HSA21 S100B contributes oxidative stress apoptosis in DS human neural progenitors (HNPs). Here we show HNPs isolated from fetal frontal cortex demonstrate not only disturbances redox states within the...

10.1371/journal.pone.0022126 article EN cc-by PLoS ONE 2011-07-11
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