Cargando…

Abolishing Tau cleavage by caspases at Aspartate(421) causes memory/synaptic plasticity deficits and pre-pathological Tau alterations

TAU mutations are genetically linked to fronto-temporal dementia (FTD) and hyper-phosphorylated aggregates of Tau form neurofibrillary tangles (NFTs) that constitute a pathological hallmark of Alzheimer disease (AD) and FTD. These observations indicate that Tau has a pivotal role in the pathogenesis...

Descripción completa

Detalles Bibliográficos
Autores principales:	Biundo, F, d'Abramo, C, Tambini, M D, Zhang, H, Del Prete, D, Vitale, F, Giliberto, L, Arancio, O, D'Adamio, L
Formato:	Online Artículo Texto
Lenguaje:	English
Publicado:	Nature Publishing Group 2017
Materias:	Original Article
Acceso en línea:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5611732/ https://www.ncbi.nlm.nih.gov/pubmed/28786980 http://dx.doi.org/10.1038/tp.2017.165

Ejemplares similares

Correction: Abolishing Tau cleavage by caspases at Aspartate(421) causes memory/synaptic plasticity deficits and pre-pathological Tau alterations
por: Biundo, F., et al.
Publicado: (2018)

A role for tau in learning, memory and synaptic plasticity
por: Biundo, Fabrizio, et al.
Publicado: (2018)

Significance of Blood and Cerebrospinal Fluid Biomarkers for Alzheimer’s Disease: Sensitivity, Specificity and Potential for Clinical Use
por: d’Abramo, Cristina, et al.
Publicado: (2020)

Intramuscular injection of vectorized-scFvMC1 reduces pathological tau in two different tau transgenic models
por: Vitale, Francesca, et al.
Publicado: (2020)

Anti-tau conformational scFv MC1 antibody efficiently reduces pathological tau species in adult JNPL3 mice
por: Vitale, Francesca, et al.
Publicado: (2018)

Aβ43 levels determine the onset of pathological amyloid deposition
por: Tambini, Marc D., et al.
Publicado: (2023)

Transgenic Expression of the Amyloid-β Precursor Protein-Intracellular Domain Does Not Induce Alzheimer's Disease–Like Traits In Vivo
por: Giliberto, Luca, et al.
Publicado: (2010)

Hyperphosphorylation and Cleavage at D421 Enhance Tau Secretion
por: Plouffe, Vanessa, et al.
Publicado: (2012)

An Intracellular Threonine of Amyloid-β Precursor Protein Mediates Synaptic Plasticity Deficits and Memory Loss
por: Lombino, Franco, et al.
Publicado: (2013)

Facilitation of glutamate, but not GABA, release in Familial Alzheimer's APP mutant Knock‐in rats with increased β‐cleavage of APP
por: Tambini, Marc D., et al.
Publicado: (2019)

Caspase-9 mediates synaptic plasticity and memory deficits of Danish dementia knock-in mice: caspase-9 inhibition provides therapeutic protection
por: Tamayev, Robert, et al.
Publicado: (2012)

Cleavage of human tau at Asp421 inhibits hyperphosphorylated tau induced pathology in a Drosophila model
por: Chi, Hao, et al.
Publicado: (2020)

A driver or a passenger? D421-caspase cleaved tau is associated with aggregated and insoluble tau
por: Gibson, Yolanda, et al.
Publicado: (2013)

Trem2 Splicing and Expression are Preserved in a Human Aβ-producing, Rat Knock-in Model of Trem2-R47H Alzheimer’s Risk Variant
por: Tambini, Marc D., et al.
Publicado: (2020)

Knock-in rats with homozygous PSEN1(L435F) Alzheimer mutation are viable and show selective γ-secretase activity loss causing low Aβ40/42 and high Aβ43
por: Tambini, Marc D., et al.
Publicado: (2020)

Deletion of the γ-secretase subunits Aph1B/C impairs memory and worsens the deficits of knock-in mice modeling the Alzheimer-like familial Danish dementia
por: Biundo, Fabrizio, et al.
Publicado: (2016)

Synaptic and memory dysfunction induced by tau oligomers is rescued by up-regulation of the nitric oxide cascade
por: Acquarone, Erica, et al.
Publicado: (2019)

β- but not γ-secretase proteolysis of APP causes synaptic and memory deficits in a mouse model of dementia
por: Tamayev, Robert, et al.
Publicado: (2012)

Opposite changes in APP processing and human Aβ levels in rats carrying either a protective or a pathogenic APP mutation
por: Tambini, Marc D, et al.
Publicado: (2020)

LTP and memory impairment caused by extracellular Aβ and Tau oligomers is APP-dependent
por: Puzzo, Daniela, et al.
Publicado: (2017)

Generation and Initial Characterization of FDD Knock In Mice
por: Giliberto, Luca, et al.
Publicado: (2009)

The Familial dementia gene ITM2b/BRI2 facilitates glutamate transmission via both presynaptic and postsynaptic mechanisms
por: Yao, Wen, et al.
Publicado: (2019)

Passive Immunization in JNPL3 Transgenic Mice Using an Array of Phospho-Tau Specific Antibodies
por: d’Abramo, Cristina, et al.
Publicado: (2015)

Tau Passive Immunotherapy in Mutant P301L Mice: Antibody Affinity versus Specificity
por: d’Abramo, Cristina, et al.
Publicado: (2013)

APP Is Cleaved by Bace1 in Pre-Synaptic Vesicles and Establishes a Pre-Synaptic Interactome, via Its Intracellular Domain, with Molecular Complexes that Regulate Pre-Synaptic Vesicles Functions
por: Del Prete, Dolores, et al.
Publicado: (2014)

Activity-dependent tau cleavage by caspase-3 promotes neuronal dysfunction and synaptotoxicity
por: Opland, Carli K., et al.
Publicado: (2023)

The molecular implications of a caspase-2-mediated site-specific tau cleavage in tauopathies
por: Liu, Peng, et al.
Publicado: (2021)

Alzheimer’s disease: Ablating single master site abolishes tau hyperphosphorylation
por: Stefanoska, Kristie, et al.
Publicado: (2022)

Microglia TREM2(R47H) Alzheimer-linked variant enhances excitatory transmission and reduces LTP via increased TNF-α levels
por: Ren, Siqiang, et al.
Publicado: (2020)

Late-long-term potentiation magnitude, but not Aβ levels and amyloid pathology, is associated with behavioral performance in a rat knock-in model of Alzheimer disease
por: Yesiltepe, Metin, et al.
Publicado: (2022)

Extracellular Tau Oligomers Produce An Immediate Impairment of LTP and Memory
por: Fá, M., et al.
Publicado: (2016)

APP and APLP2 interact with the synaptic release machinery and facilitate transmitter release at hippocampal synapses
por: Fanutza, Tomas, et al.
Publicado: (2015)

Tau and Caspase 3 as Targets for Neuroprotection
por: Idan-Feldman, Anat, et al.
Publicado: (2012)

β - but not γ-secretase proteolysis of APP causes synaptic and memory deficits in a mouse model of dementia
por: Tamayev, Robert, et al.
Publicado: (2012)

Transfixed by transgenics: how pathology assumptions are slowing progress in Alzheimer's disease and related dementia research
por: D'Adamio, Luciano
Publicado: (2023)

Evidence that the Amyloid beta Precursor Protein-intracellular domain lowers the stress threshold of neurons and has a "regulated" transcriptional role
por: Giliberto, Luca, et al.
Publicado: (2008)

Updated Measurement of the \tau Polarisation in \tau -> \tau(K)\nu_\tau
por: Moraes, D, et al.
Publicado: (1998)

Amphiphysin I cleavage by asparagine endopeptidase leads to tau hyperphosphorylation and synaptic dysfunction
por: Zhang, Xingyu, et al.
Publicado: (2021)

Caspase-Mediated Truncation of Tau Potentiates Aggregation
por: Lee, Sangmook, et al.
Publicado: (2012)

Tyr(682) in the Intracellular Domain of APP Regulates Amyloidogenic APP Processing In Vivo
por: Barbagallo, Alessia P. M., et al.
Publicado: (2010)

Cannot write session to /tmp/vufind_sessions/sess_gunjdhas7ris7u6klnb8it1iv1