Search results for: Alessandra Piccini

Items from 1 to 14 out of 14 results

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Altered Intracellular Calcium Homeostasis Underlying Enhanced Glutamatergic Transmission in Striatal-Enriched Tyrosine Phosphatase (STEP) Knockout Mice

Federica Bosco, Pierluigi Valente, Marco Milanese, Alessandra Piccini, more

Molecular Neurobiology > 2018 > 55 > 10 > 8084-8102

The striatal-enriched protein tyrosine phosphatase (STEP) is a brain-specific phosphatase involved in synaptic transmission. The current hypothesis on STEP function holds that it opposes synaptic strengthening by dephosphorylating and inactivating key neuronal proteins involved in synaptic plasticity and intracellular signaling, such as the MAP kinases ERK1/2 and p38, as well as the tyrosine kinase...

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APache Is an AP2-Interacting Protein Involved in Synaptic Vesicle Trafficking and Neuronal Development

Alessandra Piccini, Enrico Castroflorio, Pierluigi Valente, Fabrizia C. Guarnieri, more

Cell Reports > 2017 > 21 > 12 > 3596-3611

Synaptic transmission is critically dependent on synaptic vesicle (SV) recycling. Although the precise mechanisms of SV retrieval are still debated, it is widely accepted that a fundamental role is played by clathrin-mediated endocytosis, a form of endocytosis that capitalizes on the clathrin/adaptor protein complex 2 (AP2) coat and several accessory factors. Here, we show that the previously uncharacterized...

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Synapsin III Acts Downstream of Semaphorin 3A/CDK5 Signaling to Regulate Radial Migration and Orientation of Pyramidal Neurons In Vivo

Laura E. Perlini, Joanna Szczurkowska, Bryan A. Ballif, Alessandra Piccini, more

Cell Reports > 2015 > 11 > 2 > 234-248

Synapsin III (SynIII) is a phosphoprotein that is highly expressed at early stages of neuronal development. Whereas in vitro evidence suggests a role for SynIII in neuronal differentiation, in vivo evidence is lacking. Here, we demonstrate that in vivo downregulation of SynIII expression affects neuronal migration and orientation. By contrast, SynIII overexpression affects neuronal migration, but...

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Monomeric Aβ1–42 and RAGE: key players in neuronal differentiation

Sabrina Piras, Anna L. Furfaro, Alessandra Piccini, Mario Passalacqua, more

Neurobiology of Aging > 2014 > 35 > 6 > 1301-1308

The aggregation of amyloid-β (Aβ) peptides plays a crucial role in the onset and progression of Alzheimer's disease. Monomeric form of Aβ, indeed, could exert a physiological role. Considering the anti-oligomerization property of all-trans retinoic acid (ATRA), the involvement of monomeric Aβ1–42 in ATRA-induced neuronal differentiation has been investigated. Four-day ATRA treatment increases β-secretase...

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β‐Amyloid 1‐42 induces physiological transcriptional regulation of BACE1

Alessandra Piccini, Roberta Borghi, Michela Guglielmotto, Elena Tamagno, more

Journal of Neurochemistry > 122 > 5 > 1023 - 1031

J. Neurochem. (2012) 122, 1023–1031. AbstractThe pathogenesis of Alzheimer’s disease (AD) is only partially understood. β‐amyloid (Aβ) is physiologically generated by sequential cleavage of its precursor protein by the β‐ and the γ‐secretase and it is normally disposed of. In Alzheimer’s disease, Aβ is excessively produced or less dismissed, but the hypothesis on its physiological and pathological...

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Mapping brain morphological and functional conversion patterns in amnestic MCI: a voxel-based MRI and FDG-PET study

Silvia Morbelli, Arnoldo Piccardo, Giampiero Villavecchia, Barbara Dessi, more

European Journal of Nuclear Medicine and Molecular Imaging > 2010 > 37 > 1 > 36-45

Purpose To reveal the morphological and functional substrates of memory impairment and conversion to Alzheimer disease (AD) from the stage of amnestic mild cognitive impairment (aMCI). Methods Brain MRI and FDG-PET were performed in 20 patients with aMCI and 12 controls at baseline. During a mean follow-up of about 2 years, 9 patients developed AD (converters), and 11 did not (nonconverters). All...

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Effect on memory of acute administration of naturally secreted fibrils and synthetic amyloid-beta peptides in an invertebrate model

Mariana Feld, Cinzia Galli, Alessandra Piccini, Arturo Romano

Neurobiology of Learning and Memory > 2008 > 89 > 4 > 407-418

Amyloid β peptide (Aβ) is considered one of the main agents of Alzheimer’s disease pathogenesis. Recently, it has been proposed that memory deficits are caused by different stages of Aβ aggregation, particularly by oligomers. In addition, although memory impairment was found after Aβ administration in rodents and chicks, the nature of the memory deficits induced in invertebrates by acute administration...

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The increased activity of BACE1 correlates with oxidative stress in Alzheimer's disease

Roberta Borghi, Stefania Patriarca, Nicola Traverso, Alessandra Piccini, more

Neurobiology of Aging > 2007 > 28 > 7 > 1009-1014

We evaluated expression, protein levels and activity of the β-site cleaving enzyme (BACE1) as well as the amount of products of lipid peroxidation in frontal cortex of three groups of cases: sporadic Alzheimer's disease (AD); control subjects (CTR); cognitively normal subjects with abundant amyloid plaques (NA). We found a significant increase of BACE1 activity and products of lipid peroxidation in...

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A cerebellar variant of Alzheimer’s disease caused by presenilin 1 S170F mutation

Alessandra Piccini, Gianluigi Zanusso, Roberta Borghi, Cristiana Noviello, more

Alzheimer's & Dementia: The Journal of the Alzheimer's Association > 2006 > 2 > 3 Supplement > S499

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Neprylisin decreases uniformly in Alzheimer’s disease and in normal aging

Roberta Russo, Roberta Borghi, William Markesbery, Massimo Tabaton, more

FEBS Letters > 2005 > 579 > 27 > 6027-6030

The proteolysis of β-amyloid (Aβ) requires neprylisin, an enzyme that has been shown as reduced in Alzheimer’s disease (AD). We investigated whether a decrease in neprilysin levels contributes to the accumulation of amyloid deposits not only in AD but also in the normal aging. We analyzed neprilysin mRNA and protein levels in cerebral cortex from 10 cognitively normal elderly subjects with amyloid...

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Protein levels of glycogen synthase 3 kinase are normal in progressive supranuclear palsy

Roberta Borghi, Alessandra Piccini, Andrè Delacourte, Paola Strocchi, more

Neuroscience Letters > 2004 > 366 > 1 > 67-70

Progressive supranuclear palsy (PSP) is a neurodegenerative disorder characterized by pure neurofibrillary tau pathology involving mainly basal ganglia and brain stem nuclei. One of the kinases involved in tau phosphorylation is glycogen synthase 3 kinase (GSK3). In mammals GSK3 is present in two isoforms, α and β regulated by phosphorylation: phosphorylation of Ser9 in GSK3β or Ser21 in GSK3α leads...

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P1-167 Soluble abeta shows a different composition in normal aging and Alzheimer's disease

Alessandra Piccini, Antonella Vitali, Roberta Borghi, Luca Giliberto, more

Neurobiology of Aging > 2004 > 25 > Supplement 2 > S143

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P2-261 Plasma levels of amyloid beta-protein 42 are increased in women with mild cognitive impairment

Luca Giliberto, Andrea Assini, Sergio Cammarata, Monica Colucci, more

Neurobiology of Aging > 2004 > 25 > Supplement 2 > S306-S307

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Fibroblasts from FAD-linked presenilin 1 mutations display a normal unfolded protein response but overproduce Aβ42 in response to tunicamycin

Alessandra Piccini, Anna Fassio, Elena Pasqualetto, Antonella Vitali, more

Neurobiology of Disease > 2004 > 15 > 2 > 380-386

Many patients affected by early onset familial Alzheimer's disease (FAD), carry mutations in the presenilin 1 (PS1) gene. Since it has been suggested that FAD-linked PS1 mutations impair the unfolded protein response (UPR) due to endoplasmic reticulum (ER) stress, we analyzed the UPR and amyloid β-protein processing in fibroblasts bearing various PS1 mutations. Neither in normal conditions nor after...

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