Maria C. Morale

ORCID: 0000-0003-0624-7234
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Stress Responses and Cortisol
  • Hypothalamic control of reproductive hormones
  • Neuroendocrine regulation and behavior
  • Neurogenesis and neuroplasticity mechanisms
  • Nuclear Receptors and Signaling
  • Nerve injury and regeneration
  • Parkinson's Disease Mechanisms and Treatments
  • Growth Hormone and Insulin-like Growth Factors
  • Immune Cell Function and Interaction
  • Receptor Mechanisms and Signaling
  • Adrenal Hormones and Disorders
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Neuropeptides and Animal Physiology
  • Reproductive System and Pregnancy
  • Cytokine Signaling Pathways and Interactions
  • Immune Response and Inflammation
  • T-cell and B-cell Immunology
  • Tryptophan and brain disorders
  • Hormonal Regulation and Hypertension
  • Genetics and Neurodevelopmental Disorders
  • Adenosine and Purinergic Signaling
  • Birth, Development, and Health
  • Phagocytosis and Immune Regulation
  • Adipose Tissue and Metabolism
  • Diet and metabolism studies

Oasi Maria SS
2005-2020

Istituti di Ricovero e Cura a Carattere Scientifico
2007-2020

Scripps Research Institute
2005-2007

Neurological Research Institute
2006

University of Trieste
2004

University of Washington
2004

University of Catania
1983-1996

University of Palermo
1990

Reduction of core body temperature has been proposed to contribute the increased life span and antiaging effects conferred by calorie restriction (CR). Validation this hypothesis difficult in homeotherms, primarily due a lack experimental models. We report that transgenic mice engineered overexpress uncoupling protein 2 hypocretin neurons (Hcrt-UCP2) have elevated hypothalamic temperature. The local elevation on central thermostat resulted 0.3° 0.5°C reduction Fed ad libitum, Hcrt-UCP2 had...

10.1126/science.1132191 article EN Science 2006-11-03

Abstract Background Dopamine-synthesizing (dopaminergic, DA) neurons in the ventral midbrain (VM) constitute a pivotal neuronal population controlling motor behaviors, cognitive and affective brain functions, which generation critically relies on activation of Wingless-type MMTV integration site (Wnt)/β-catenin pathway their progenitors. In Parkinson's disease, DA cell bodies within substantia nigra pars compacta (SNpc) progressively degenerate, with causes mechanisms poorly understood....

10.1186/1750-1326-6-49 article EN cc-by Molecular Neurodegeneration 2011-07-13

In Parkinson's disease (PD), neurogenesis is impaired in the subventricular zone (SVZ) of postmortem human PD brains, primate nonhuman and rodent models PD. The vital role Wingless-type MMTV integration site (Wnt)/β-catenin signaling modulation neurogenesis, neuroprotection, synaptic plasticity coupled to our recent findings uncovering an active for inflammation Wnt/β-catenin MPTP-induced loss repair nigrostriatal dopaminergic (DAergic) neurons prompted us study impact neuroinflammation...

10.1523/jneurosci.5259-11.2012 article EN cc-by-nc-sa Journal of Neuroscience 2012-02-08

Wnt/β-catenin signaling is required for specification and neurogenesis of midbrain dopaminergic (mDA) neurons, the pivotal neuronal population that degenerates in Parkinson's disease (PD), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model PD. plays a vital role adult but whether it might engage DA neurogenesis/neurorepair affected PD brain yet unresolved. Recently, aqueduct periventricular regions (Aq-PVRs) were shown to harbor multipotent clonogenic neural stem/progenitor...

10.1002/stem.1708 article EN Stem Cells 2014-03-20

Unconjugated bilirubin (UCB) causes encephalopathy in severely jaundiced neonates by damaging astrocytes and neurons. Astrocytes, which help defend the brain against cytotoxic insults, express ATP-dependent transporter, multidrug resistance-associated protein 1 (Mrp1), mediates export of organic anions, probably including UCB. We therefore studied whether exposure to UCB affects expression intracellular localization Mrp1 cultured mouse astroglial cells (>95% astrocytes). was localized...

10.1073/pnas.0308452100 article EN Proceedings of the National Academy of Sciences 2004-02-17

The presence of specific LHRH-binding sites within the rat thymus gland and ability LHRH its agonistic antagonistic analogs to directly modulate function prompted us study possible changes in number thymic during aging-induced physiological immunosenescence. Moreover, effects chronic treatment aging rats with a potent agonist (LHRH-A) on receptors, weight histology, as well thymocyte proliferative capacity were assessed. For comparison, castration same parameters was also investigated....

10.1210/endo-125-2-1037 article EN Endocrinology 1989-08-01

Aging and exposure to environmental toxins including MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) are strong risk factors for developing Parkinson's disease (PD), a common neurologic disorder characterized by selective degeneration of midbrain dopaminergic (DAergic) neurons astrogliosis. PD impair the subventricular zone (SVZ), one most important brain regions adult neurogenesis. Because inflammation oxidative stress hallmarks aging PD, we investigated nature, timing, signaling...

10.1523/jneurosci.3206-12.2013 article EN cc-by-nc-sa Journal of Neuroscience 2013-01-23

The development of the thymus and hypothalamic- pituitary-gonadal axis are linked by bidirectional hormonally mediated relationships. In present study, direct involvement neuropeptide LHRH in maturation cell-mediated humoral immune responses were assessed after treatment neonatal (from post-natal day 1-day 5) female rats with a potent LHRHantagonist (LHRH-anta, p-Glu-D-Phe 2,6,Pro3-LHRH, 50 μg/rat), effects compared to those resulting from castration. Whereas control animals mitogenic...

10.1210/endo-128-2-1073 article EN Endocrinology 1991-02-01

Abstract Oxidative stress is implicated in the death of dopaminergic neurons sporadic forms Parkinson's disease. Because oxidative can be modulated endogenously by uncoupling proteins (UCPs), we hypothesized that specific neuronal expression UCP2, one member UCP family rapidly induced CNS following insults, could confer neuroprotection a mouse model We generated transgenic mice overexpressing UCP2 catecholaminergic under control tyrosine hydroxylase promoter (TH‐UCP2). In these mice,...

10.1111/j.1471-4159.2005.03052.x article EN Journal of Neurochemistry 2005-03-16

The present study was designed to explore the effects of LHRH and its agonists on immune system function. As a first step, identify putative site action, very potent stable agonist (LHRH-A), [D-Ser(TBU6)] des-Gly10-LHRH ethylamide (buserelin), used as an iodinated ligand characterize receptors in membrane preparation rat thymus, key organ system. LHRH-A were then investigated proliferative capacity thymocytes exposed vitro mitogen ornithine decarboxylase specific activity. In addition,...

10.1210/endo-125-2-1025 article EN Endocrinology 1989-08-01

The marked modulation of lymphocyte function exerted by the hypothalamic decapetide LHRH prompted us to study possible involvement neuropeptide in one major steps proliferation, namely expression interleukin-2 (IL-2) receptor during vitro treatment rat lymphocytes with agonists (LHRH-A) or antagonists (LHRH-ANTA). basal proliferative activity splenocytes and thymocytes from proestrous female rats was significantly stimulated after incubation LHRH-A, but not fragments [LHRH-(1-3), LHRH-(1-5),...

10.1210/endo-129-1-277 article EN Endocrinology 1991-07-01

Current evidence suggests a role of neuroinflammation in the pathogenesis Parkinson's disease (PD) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model basal ganglia injury. Reportedly, nonsteroidal anti-inflammatory drugs (NSAIDs) mitigate DAergic neurotoxicity rodent models PD. Consistent with these findings, epidemiological analysis indicated that certain NSAIDs may prevent or delay progression However, serious impediment chronic NSAID therapy, particularly elderly, is gastric,...

10.1186/1742-2094-7-83 article EN cc-by Journal of Neuroinflammation 2010-11-23

We used transgenic mice with impaired corticosteroid receptor function, caused by expression of type II glucocorticoid (GR) antisense RNA, to study the role feedback during developmental maturation hypothalamus-pituitary-adrenal-immune functions. These have increased plasma concentrations ACTH and corticosterone as well reduced GR binding capacity. In control mice, a strong sex dimorphism in development gene is apparent, males between postnatal days 9-36, transcript concentration...

10.1210/endo.136.9.7649104 article EN Endocrinology 1995-09-01

Glucocorticoids (GCs) exert via glucocorticoid receptors (GRs) potent anti-inflammatory and immunosuppressive effects. Emerging evidence indicates that an inflammatory process is involved in dopaminergic nigro-striatal neuronal loss Parkinson's disease. We here report the GR deficiency of transgenic (Tg) mice expressing antisense RNA from early embryonic life has a dramatic impact "programming" vulnerability neurons to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The Tg exacerbates...

10.1096/fj.03-0501fje article EN The FASEB Journal 2003-11-20
Coming Soon ...