ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Selective hippocampal neurodegeneration in transgenic mice expressing small amounts of truncated Aβ is induced by pyroglutamate-Aβ formation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 103 citations in OpenAlex.
- High-Fat Diet and a High Amyloid Load Interact to Induce PKC-α Dependent Synaptic Insulin Resistance.Molecular & cellular proteomics : MCP · 2026Article
- Immunomodulatory functions of glutaminyl cyclases QPCTL and QPCT.Frontiers in immunology · 2026Review
- Monomers, Dimers, and Oligomers of Pyroglutamate-Modified α-Synuclein Fragments Exhibit Distinct Biophysical Characteristics.ACS chemical neuroscience · 2025Article
- Effects of chronic empathic stress on synaptic efficacy, as well as short-term and long-term plasticity at the Schaffer collateral/commissural- CA1 synapses in the dorsal hippocampus of rats.Metabolic brain disease · 2024Article
- Identification of isoAsp7-Aβ as a major Aβ variant in Alzheimer's disease, dementia with Lewy bodies and vascular dementia.Acta neuropathologica · 2024Article
- Article
- Jacob-induced transcriptional inactivation of CREB promotes Aβ-induced synapse loss in Alzheimer's disease.The EMBO journal · 2023Article
- Pyroglutamate Aβ cascade as drug target in Alzheimer's disease.Molecular psychiatry · 2022Review
- Neddylation-dependent protein degradation is a nexus between synaptic insulin resistance, neuroinflammation and Alzheimer's disease.Translational neurodegeneration · 2022Article
- Sex-Related Motor Deficits in the Tau-P301L Mouse Model.Biomedicines · 2021Article
- A glutaminyl cyclase-catalyzed α-synuclein modification identified in human synucleinopathies.Acta neuropathologica · 2021Article
- PEAβ Triggers Cognitive Decline and Amyloid Burden in a Novel Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2021Article
- Proteolytic α-Synuclein Cleavage in Health and Disease.International journal of molecular sciences · 2021Review
- Article
- Prediction of Cerebral Amyloid Pathology Based on Plasma Amyloid and Tau Related Markers.Frontiers in neurology · 2021Article
- Mendelian randomization integrating GWAS and mQTL data identified novel pleiotropic DNA methylation loci for neuropathology of Alzheimer's disease.Neurobiology of aging · 2021Article
- Neuron Loss in Alzheimer's Disease: Translation in Transgenic Mouse Models.International journal of molecular sciences · 2020Review
- Transgene integration causes RARB downregulation in homozygous Tg4-42 mice.Scientific reports · 2020Article
- Correlation of pyroglutamate amyloid β and ptau Ser202/Thr205 levels in Alzheimer's disease and related murine models.PloS one · 2020Article
- Reduced Acoustic Startle Response and Prepulse Inhibition in the Tg4-42 Model of Alzheimer's Disease.Journal of Alzheimer's disease reports · 2019Article
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Authors and funding
19 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Posttranslational amyloid-β (Aβ) modification is considered to play an important role in Alzheimer's disease (AD) etiology. An N-terminally modified Aβ species, pyroglutamate-amyloid-β (pE3-Aβ), has been described as a major constituent of Aβ deposits specific to human AD but absent in normal aging. Formed via cyclization of truncated Aβ species by glutaminyl cyclase (QC; QPCT) and/or its isoenzyme (isoQC; QPCTL), pE3-Aβ aggregates rapidly and is known to seed additional Aβ aggregation. To directly investigate pE3-Aβ toxicity in vivo, we generated and characterized transgenic TBA2.1 and TBA2.2 mice, which express truncated mutant human Aβ. Along with a rapidly developing behavioral phenotype, these mice showed progressively accumulating Aβ and pE3-Aβ deposits in brain regions of neuronal loss, impaired long-term potentiation, microglial activation, and astrocytosis. Illustrating a threshold for pE3-Aβ neurotoxicity, this phenotype was not found in heterozygous animals but in homozygous TBA2.1 or double-heterozygous TBA2.1/2.2 animals only. A significant amount of pE3-Aβ formation was shown to be QC-dependent, because crossbreeding of TBA2.1 with QC knock-out, but not isoQC knock-out, mice significantly reduced pE3-Aβ levels. Hence, lowering the rate of QC-dependent posttranslational pE3-Aβ formation can, in turn, lower the amount of neurotoxic Aβ species in AD.
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