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| 1 | NF-kappaB dimers in the regulation of neuronal survival显示文摘 | Sarnico I Lanzillotta A Benarese M | 2009 | Int Rev Neurobiol2009，85，： | 1 |
| 2 | NF-kappaB dimers in the regulation of neuronal survival 显示文摘 | Sarnico I Lanzillotta A Benarese M | 2009 | Int Rev Neurobiol2009，85，： | 1 |
| 3 | The inhibitor of I kappa B alpha phosphorylation BAY 11-7082 prevents NMDA neurotoxicity in mouse hippocampal slices显示文摘 | GOFFI F BORONI F BENARESE M | | 0，，： | 1 |
| 4 | NF-кB pathway:a target for preventing b-amyloid (Ab)-induced neuronal damage and Ab42 production显示文摘 | VALERIO A BORONI F BENARESE M | 2006 | Eur J Neur2006，23，： | 1 |
| 5 | NF - kappaB pathway : a Target for preventing beta - amyloid (Abeta) - induced neuronal damage and Abeta42 prod - uction 显示文摘 | Valerio A Boroni F Benarese M | 2006 | Eur J Neurosci2006，23，： | 1 |
| 6 | Prevention of neuron and oligodendrocyte degeneration by interleukin-6 (IL-6) and IL-6 receptor/IL-6 fusion protein in organotypic hippocampal slices显示文摘 | Marina Pizzi Ilenia Sarnico Flora Boroni Marina Benarese Michel Dreano Gianni Garotta Alessandra Valerio PierFranco Spano | 2003 | Molecular and Cellular Neuroscience2003，，2： | 1 |
| 7 | NF-kappaB path- way:a target for preventing beta-amyloid (Ab)-induced neuronal damage and Abeta42 production 显示文摘 | Valerio A Boroni F Benarese M | 2006 | Eur J Neurosci2006，23，7： | 1 |
| 8 | NF-kappaB pathway:a target for preventing beta-amyloid (Abeta)-induced neuronal damageand Abeta42 production显示文摘 | Valerio A Boroni F Benarese M | 2006 | Eur J Neurosci2006，23，： | 1 |
| 9 | NF-kappaB pathway : a target for preventing beta-amyloid (Abeta)-induced and neuronal damage Abe-ta42 production 显示文摘 | Valerio A Boroni F Benarese M | 2006 | Eur J Neurosci2006，23，7： | 1 |
| 10 | NF-kapppaB pathway:a target for preventing betaamyloid (Abeta)-induced and neuroal damage Abeta42 production显示文摘 | Valerio A Boronl F Benarese M | | 0，，07： | 1 |
| 11 | NF-kappaB pathway:a target for preventing beta-amyloid (Abeta)-induced neuronal damage and Abeta42 production显示文摘 | Valerio A Boroni F Benarese M | 2006 | Eur J Neurosci2006，23，7： | 1 |
| 12 | NF-κB pathway:atarget for preventing b-amyloid(Ab)-inducedneuronaldam-age and,Abeta42production显示文摘 | Valerio A Boroni F Benarese M | 2006 | Neurosci2006，23，7： | 1 |
| 13 | NF-κB/c-Rel deficiency causes Parkinson’s disease-like prodromal symptoms and progressive pathology in mice显示文摘Background:Parkinson’s disease(PD),the most common neurodegenerative movement disorder,is characterized by dopaminergic nigrostriatal neuron loss and brain accumulation of Lewy bodies,protein aggregates mainly composed ofα-synuclein.We reported that mice deficient for NF-κB/c-Rel(c-rel^(-/-))develop a late-onset parkinsonism.At 18 months of age,c-rel^(-/-)mice showed nigrostriatal degeneration and accumulation ofα-synuclein aggregates associated with a motor impairment responsive to L-DOPA administration.Being c-Rel protein a transcriptional regulator for mitochondrial anti-oxidant and antiapoptotic factors,it has been inferred that its deficiency may affect the resilience of“energy demanding”nigral dopaminergic neurons to the aging process.PD patients manifest a prodromal syndrome that includes olfactory and gastrointestinal dysfunctions years before the frank degeneration of nigrostriatal neurons and appearance of motor symptoms.According to the Braak staging,the onset of non-motor and motor symptoms relates to progressive ascendant diffusion ofα-synuclein pathology in the brain.The aim of this study was to identify whether c-rel^(-/-)deficiency is associated with the onset of premotor signs of PD and spatio-temporal progression of cerebralα-synuclein deposition.Methods:Intestinal and olfactory functions,intestine and brainα-synuclein deposition as well as striatal alterations,were assessed in c-rel^(-/-)and control mice from 2 to 18 months of age.Results:From 2 months of age,c-rel^(-/-)mice displayed intestinal constipation and increasing olfactory impairment.At 2 months,c-rel^(-/-)mice exhibited a mildα-synuclein accumulation in the distal colon.Moreover,they developed an agedependent deposition of fibrillaryα-synuclein that,starting at 5 months from the olfactory bulbs,dorsal motor nucleus of vagus and locus coeruleus,reached the substantia nigra at 12 months.At this age,theα-synuclein pathology associated with a drop of dopamine transporter in the striatum that anticipated by 6 months the axonal degeneration.From 12 months onwards oxidative/nitrosative stress developed in the striatum in parallel with altered expression of mitochondrial homeostasis regulators in the substantia nigra.Conclusions:In c-rel^(-/-)mice,reproducing a parkinsonian progressive pathology with non-motor and motor symptoms,a Braak-like pattern of brain ascendingα-synuclein deposition occurs.The peculiar phenotype of c-rel^(-/-)mice envisages a potential contribution of c-Rel dysregulation to the pathogenesis of PD. | Edoardo Parrella Arianna Bellucci Vanessa Porrini Marina Benarese Annamaria Lanzillotta Gaia Faustini Francesca Longhena Giulia Abate Daniela Uberti Marina Pizzi | 2019 | Translational Neurodegeneration2019，8，1： | 1 |
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