Tiziana Pascucci

ORCID: 0000-0003-1520-7373
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About
Contact & Profiles
Research Areas
  • Metabolism and Genetic Disorders
  • Autism Spectrum Disorder Research
  • Genetics and Neurodevelopmental Disorders
  • Stress Responses and Cortisol
  • Neuroscience and Neuropharmacology Research
  • Neuroendocrine regulation and behavior
  • Neurotransmitter Receptor Influence on Behavior
  • Diet and metabolism studies
  • Mitochondrial Function and Pathology
  • Adipose Tissue and Metabolism
  • Receptor Mechanisms and Signaling
  • Neurogenesis and neuroplasticity mechanisms
  • Child Nutrition and Feeding Issues
  • Amino Acid Enzymes and Metabolism
  • RNA regulation and disease
  • Child and Adolescent Psychosocial and Emotional Development
  • Parkinson's Disease Mechanisms and Treatments
  • Virology and Viral Diseases
  • Regulation of Appetite and Obesity
  • Mental Health Treatment and Access
  • Metabolomics and Mass Spectrometry Studies
  • Neuroscience and Neural Engineering
  • Folate and B Vitamins Research
  • Anxiety, Depression, Psychometrics, Treatment, Cognitive Processes
  • Circadian rhythm and melatonin

Sapienza University of Rome
2015-2025

Fondazione Santa Lucia
2015-2024

Istituti di Ricovero e Cura a Carattere Scientifico
2002-2024

European Brain Research Institute
2008-2015

Laboratoire de Neurosciences Cognitives
2005

Università Campus Bio-Medico
2004

Istituto Superiore di Sanità
2001

Istituto Psicoanalitico per le Ricerche Sociali
2000

Institute of Molecular Biology and Pathology
1999

Marquette University
1996

Thalamocortical neurons innervating the barrel cortex in neonatal rodents transiently store serotonin (5-HT) synaptic vesicles by expressing plasma membrane transporter (5-HTT) and vesicular monoamine (VMAT2). 5-HTT knock-out (ko) mice reveal a nearly complete absence of 5-HT cerebral immunohistochemistry, barrels, both at P7 adulthood. Quantitative electron microscopy reveals that ko affects neither density synapses nor length contacts layer IV. VMAT2 mice, completely lacking...

10.1523/jneurosci.21-17-06862.2001 article EN Journal of Neuroscience 2001-09-01

Although patients with Parkinson's disease show impairments in cognitive performance even at the early stage of disease, synaptic mechanisms underlying impairment this pathology are unknown.Hippocampal long-term potentiation represents major experimental model for changes learning and memory is controlled by endogenous dopamine.We found that hippocampal altered both a neurotoxic transgenic plastic alteration associated an impaired dopaminergic transmission decrease NR2A/NR2B subunit ratio...

10.1093/brain/aws101 article EN Brain 2012-05-04

Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder characterized by deficits in social interaction/communication, stereotypic behaviors, restricted interests, and abnormal sensory-processing. Several studies have reported significantly elevated urinary foecal levels of

10.3390/brainsci10040233 article EN cc-by Brain Sciences 2020-04-13

The vgf gene has been identified as an energy homeostasis regulator. Vgf encodes a 617-aa precursor protein that is processed to yield incompletely characterized panel of neuropeptides. Until now, it was unproved assumption VGF-derived peptides could regulate metabolism. Here, VGF peptide designated TLQP-21 in rat brain extracts by means immunoprecipitation, microcapillary liquid chromatography-tandem MS, and database searching algorithms. Chronic intracerebroventricular (i.c.v.) injection...

10.1073/pnas.0606102103 article EN Proceedings of the National Academy of Sciences 2006-09-19

Although the medial prefrontal cortex (mpFC) appears to constrain stress responses, indirect evidences suggest that it might determine response of mesoaccumbens dopamine (DA) system. To test this hypothesis, we first evaluated dynamics norepinephrine (NE) and DA release in mpFC nucleus accumbens (NAc) acutely stressed rats. Then, tested effects selective depletion NE or (by local 6-hydroxydopamine infusion following desipramine...

10.1093/cercor/bhm008 article EN Cerebral Cortex 2007-02-24

Epidemiological evidence links exposure to stressful life events with increased risk for mental illness. However, there is significant individual variability in vulnerability environmental factors, and genetic variation thought play a major role determining who will become ill. Several studies have shown, example, that individuals carrying the S (short) allele of serotonin transporter (5-HTT) gene-linked polymorphic region (5-HTTLPR) an depression following stress adulthood. Identifying...

10.1242/dmm.004614 article EN Disease Models & Mechanisms 2010-04-07

Autism is a complex neurodevelopmental disorder, likely encompassing multiple pathogenetic components. The aim of this study to begin identifying at least some these components and assess their association with biological endophenotypes. To address issue, we recruited 245 Italian patients idiopathic autism spectrum disorders first-degree relatives. Using stepwise approach, patient family history variables were analyzed using principal component analysis ("exploratory phase"), followed by...

10.1002/aur.151 article EN Autism Research 2010-09-27

Background In man, many different events implying childhood separation from caregivers/unstable parental environment are associated with heightened risk for panic disorder in adulthood. Twin data show that the occurrence of such contributes to explaining covariation between anxiety disorder, panic, and related psychobiological trait CO2 hypersensitivity. We hypothesized early interference infant-mother interaction could moderate interspecific response through genetic control sensitivity...

10.1371/journal.pone.0018637 article EN cc-by PLoS ONE 2011-04-08

Fragile X syndrome is an X-linked form of mental retardation including, among others, symptoms such as stereotypic behaviour, hyperactivity, hyperarousal, and cognitive deficits. We hypothesized that hyperactivity and/or compromised attentional, functions may lead to impaired performance in tasks Fmr1 knockout mice, the most widely used animal model fragile syndrome, suggested psychostimulant treatment improve by acting on one or both components. Since have been depend striatal prefrontal...

10.1097/00008877-200409000-00018 article EN Behavioural Pharmacology 2004-09-01

Clinical data suggest that brain catecholamines and serotonin are deficient in phenylketonuria (PKU), an inherited metabolic disorder causes severe mental retardation neurological disturbances. To test this hypothesis, tissue levels of dopamine (DA), norepinephrine (NE), 5-hydroxytryptamine (5-HT) their metabolites were evaluated the genetic mouse model PKU (Pahenu2). Results indicated a significant reduction 5-HT metabolism prefrontal cortex (pFC), cingulate (Cg), nucleus accumbens (NAc),...

10.1097/00001756-200004270-00042 article EN Neuroreport 2000-04-01

Phenylketonuria (PKU) is an autosomal recessive genetic disease caused by defects in the phenylalanine hydroxylase gene. Preclinical and clinical investigations suggest that ammonia lyase (PAL) could be effective alternative for treatment of PKU. The aim this study to investigate if erythrocytes loaded with PAL may act as a safe delivery system able overcome bioavailability issues provide, vivo, therapeutically relevant concentration enzyme. Murine were recombinant from Anabaena variabilis...

10.1016/j.jconrel.2014.08.012 article EN cc-by-nc-nd Journal of Controlled Release 2014-08-23

ABSTRACT Background : Recent studies support the therapeutic utility of repetitive transcranial magnetic stimulation in Parkinson's disease (PD), whose progression is correlated with loss corticostriatal long‐term potentiation and depression. Glial cell activation also a feature PD that gaining increasing attention field because astrocytes play role chronic neuroinflammatory responses but are able to manage dopamine (DA) levels. Methods Intermittent theta‐burst protocol was applied study...

10.1002/mds.26982 article EN Movement Disorders 2017-04-10
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