A5056468131- Neuroscience and Neuropharmacology Research
- Alzheimer's disease research and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Nuclear Receptors and Signaling
- Pain Mechanisms and Treatments
- Receptor Mechanisms and Signaling
- Cholinesterase and Neurodegenerative Diseases
- Photoreceptor and optogenetics research
- Ion channel regulation and function
- Wnt/β-catenin signaling in development and cancer
- Neurogenesis and neuroplasticity mechanisms
- Anesthesia and Neurotoxicity Research
- Mitochondrial Function and Pathology
- Photochromic and Fluorescence Chemistry
- Memory and Neural Mechanisms
- Tryptophan and brain disorders
- Chemical Synthesis and Analysis
- S100 Proteins and Annexins
- Pharmacological Effects of Natural Compounds
- Neuropeptides and Animal Physiology
- Computational Drug Discovery Methods
- RNA regulation and disease
- Biochemical effects in animals
- Cancer-related gene regulation
- Biochemical Analysis and Sensing Techniques
University of Catania
2013-2024
National Research Council
2004-2024
Institute of Crystallography
2020-2024
American Pharmacists Association
2021
Weatherford College
2021
Institute of Biostructure and Bioimaging
2005-2020
National Academies of Sciences, Engineering, and Medicine
2013
Sapienza University of Rome
2001-2002
I.R.C.C.S. Oasi Maria SS
2002
Istituto Neurologico Mediterraneo
2002
The molecular mechanism responsible for the neurodegeneration in Alzheimer disease is not known; however, accumulating evidence suggests that beta-amyloid peptide (A beta P) contributes to this degeneration. We now report synthetic A Ps trigger degeneration of cultured neurons through activation an apoptotic pathway. Neurons treated with exhibit morphological and biochemical characteristics apoptosis, including membrane blebbing, compaction nuclear chromatin, internucleosomal DNA...
The 42-aa-long β-amyloid protein—Aβ 1-42 —is thought to play a central role in the pathogenesis of Alzheimer's disease (AD) (Walsh and Selkoe, 2007). Data from AD brain (Shankar et al., 2008), transgenic APP (amyloid precursor protein)-overexpressing mice (Lesné 2006), neuronal cultures treated with synthetic Aβ peptides (Lambert 1998) indicate that self-association monomers into soluble oligomers is required for neurotoxicity. function monomeric unknown. evidence present CSF normal...
We used primary cultures of cortical neurons to examine the relationship between beta-amyloid toxicity and hyperphosphorylation tau protein, biochemical substrate for neurofibrillary tangles Alzheimer's brain. Exposure peptide (betaAP) induced expression secreted glycoprotein Dickkopf-1 (DKK1). DKK1 negatively modulates canonical Wnt signaling pathway, thus activating tau-phosphorylating enzyme glycogen synthase kinase-3beta. was at late times after betaAP exposure, its dependent on tumor...
The medium collected from cultured astrocytes transiently exposed to the group-II metabotropic glutamate (mGlu) receptor agonists (2 S ,1′ R ,2′ ,3′ )-2-(2,3-dicarboxycyclopropyl)glycine (DCG-IV) or (S)-4-carboxy-3-hydroxyphenylglycine (4C3HPG) is neuroprotective when transferred mixed cortical cultures challenged with NMDA (Bruno et al., 1997). following data indicate that this particular form of neuroprotection mediated by transforming growth factor-β (TGFβ). (1) TGFβ1 and -β2 were highly...
Knowing that expression of metabotropic glutamate 2 (mGlu2) receptors in the dorsal root ganglia is regulated by acetylation mechanisms, we examined effect two selective and chemically unrelated histone deacetylase (HDAC) inhibitors, <i>N</i>-(2-aminophenyl)-4-[<i>N</i>-(pyridine-3-ylmethoxy-carbonyl)aminomethyl]benzamide (MS-275) suberoylanilide hydroamic acid (SAHA), a mouse model persistent inflammatory pain. Although single subcutaneous injection MS-275 (3 mg/kg) or SAHA (5-50 was...
Prolonged exposure of cultured cortical cells or cerebellar granule to the residue 25-35 fragment beta-amyloid peptide (beta AP), beta AP(25-35), induced neuronal apoptosis, as revealed by morphological analysis, fluorescent chromatin staining, and immunodetection oligonucleosomes released from nucleus into cytoplasm. AP(25-35)-induced apoptosis was insensitive ionotropic glutamate receptor antagonists but substantially attenuated metabotropic (mGluR) agonist...
Abstract We investigated the expression and coupling to phospholipase C signal transduction pathway of metabotropic glutamate receptor (mGluR) subtypes by Western blot analysis agonist‐stimulated inositol monophosphate formation in several brain regions postnatal day 9 (P9) adult rats. In cerebral cortex, hippocampus, corpus striatum, olfactory bulb, cerebellum hypothalamus, level mGluR5 was greater at P9 than adulthood. The very low or absent hypothalamus. mGluR1a slightly hippocampus...
Trans-1-aminocyclopentane-1,3-dicarboxylic acid, a mixed agonist of all metabotropic glutamate receptor (mGluR) subtypes, is known to produce either neurotoxic or neuroprotective effects. We have therefore hypothesized that individual mGluR subtypes differentially affect neurodegenerative processes. Selective agonists which belong class II III, such as (2S,1'R,2'R,3'R)-2-(2,3-dicarboxycyclopropyl)-glycine (DCG-IV) (specific for mGluR4, 6 7), were highly potent and efficacious in protecting...
Prolonged exposure of cultured cortical neurons to the residue 25-35 fragment beta-amyloid protein, in presence dizocilpine, an antagonist N-methyl-D-aspartate receptor, and 6,7-dinitroquinoxaline-2,3-dione, alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate receptors, resulted expression proapoptotic protein Bax neuronal death. Beta-amyloid protein(25-35)-induced death was substantially attenuated by sigma1 receptor agonist 2-(4-morpholinethyl)1-phenylcyclohexanecarboxylate. The...
Dual orthosteric agonists of metabotropic glutamate 2 (mGlu2) and mGlu3 receptors are being developed as novel antipsychotic agents devoid the adverse effects conventional antipsychotics. Therefore, these drugs could be helpful for treatment psychotic symptoms associated with Alzheimer's disease (AD). In experimental animals, activity mGlu2/3 receptor is largely mediated by activation mGlu2 mimicked selective positive allosteric modulators (PAMs) receptors. We investigated distinct influence...