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2005 (v1)PublicationUploaded on: April 14, 2023
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2015 (v1)Publication
Synapsin III (SynIII) is a neuron-specific phosphoprotein that plays a unique role in neuronal development. SynIII is phosphorylated by cAMP-dependent protein kinase (PKA) at a highly conserved phosphorylation site and by cyclin-dependent kinase-5 (Cdk5) at a newly described site. Although SynIII is known to be involved in axon elongation in...
Uploaded on: March 27, 2023 -
2014 (v1)Publication
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Uploaded on: April 14, 2023 -
2000 (v1)Publication
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2004 (v1)Publication
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2008 (v1)Publication
IL-1beta and IL-18 are crucial mediators of inflammation, and a defective control of their release may cause serious diseases. Yet, the mechanisms regulating IL-1beta and IL-18 secretion are partially undefined. Both cytokines are produced as inactive cytoplasmic precursors. Processing to the active form is mediated by caspase-1, which is in...
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2007 (v1)Publication
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...
Uploaded on: April 14, 2023 -
2015 (v1)Publication
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,...
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2005 (v1)Publication
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Uploaded on: April 14, 2023 -
2008 (v1)Publication
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Uploaded on: March 31, 2023 -
2011 (v1)Publication
This study describes late-onset Alzheimer's disease (LOAD) in the mild cognitive impairment (MCI) stage, debuting with seizures in a 72 year-old woman. Prodromal AD was consistently diagnosed with four among amyloidosis and neurodegeneration biomarkers about 1 year after onset of seizures. Genetic assessment demonstrated apolipoprotein E ε2/ε3...
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2004 (v1)Publication
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2010 (v1)Publication
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Uploaded on: March 25, 2023 -
2005 (v1)Publication
The mechanism of neurodegeneration caused by beta-amyloid in Alzheimer disease is controversial. Neuronal toxicity is exerted mostly by various species of soluble beta-amyloid oligomers that differ in their N- and C-terminal domains. However, abundant accumulation of beta-amyloid also occurs in the brains of cognitively normal elderly people,...
Uploaded on: April 14, 2023 -
2013 (v1)Publication
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Uploaded on: April 14, 2023 -
2005 (v1)Publication
Epidemiological and experimental data suggest that type 2 diabetes (DM2) and sporadic late-onset Alzheimer's disease (AD) share a common mechanism, that is able to produce accumulation of insulin and amyloid beta 42 (Abeta42), the major pathogenic events respectively of the two conditions. In 71 non diabetic patients with amnestic mild...
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2010 (v1)Publication
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Uploaded on: April 14, 2023 -
2010 (v1)Publication
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Uploaded on: March 31, 2023 -
2009 (v1)Publication
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Uploaded on: March 31, 2023 -
2008 (v1)Publication
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Uploaded on: April 14, 2023 -
2007 (v1)Publication
Objective: To report an ataxic variant of Alzheimer disease expressing a novel molecular phenotype. Design: Description of a novel phenotype associated with a presenilin 1 mutation. Setting: The subject was an outpatient who was diagnosed at the local referral center. Patient: A 28-year-old man presented with psychiatric symptoms and...
Uploaded on: April 14, 2023 -
2008 (v1)Publication
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Uploaded on: April 14, 2023