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View article: PrP<sup>C</sup>-induced signaling in human neurons activates phospholipase Cɣ1 and an Arc/Arg3.1 response
PrP<sup>C</sup>-induced signaling in human neurons activates phospholipase Cɣ1 and an Arc/Arg3.1 response Open
Synaptic dysfunction and loss correlate with cognitive decline in neurodegenerative diseases, including Alzheimer’s disease (AD) and prion disease. Neuronal hyperexcitability occurs in the early stages of AD and experimental prion disease,…
View article: Mutant prion protein enhances NMDA receptor activity, activates PKC, and triggers rapid excitotoxicity in mice
Mutant prion protein enhances NMDA receptor activity, activates PKC, and triggers rapid excitotoxicity in mice Open
Neuronal hyperexcitability precedes synapse loss in certain neurodegenerative diseases, yet the synaptic membrane interactions and downstream signaling events remain unclear. The disordered amino terminus of the prion protein (PrPC) has be…
View article: Multi-omic analysis of meningeal cerebral amyloid angiopathy reveals enrichment of unsubstituted glucosamine and extracellular proteins
Multi-omic analysis of meningeal cerebral amyloid angiopathy reveals enrichment of unsubstituted glucosamine and extracellular proteins Open
Cerebral amyloid angiopathy (CAA) is a common feature of Alzheimer’s disease in which amyloid-β (Aβ) deposits in cerebral and leptomeningeal vessel walls, predisposing vessels to micro- and macro-hemorrhages. The vessel walls contain disti…
View article: Neuronal Ndst1 depletion accelerates prion protein clearance and slows neurodegeneration in prion infection
Neuronal Ndst1 depletion accelerates prion protein clearance and slows neurodegeneration in prion infection Open
Select prion diseases are characterized by widespread cerebral plaque-like deposits of amyloid fibrils enriched in heparan sulfate (HS), a abundant extracellular matrix component. HS facilitates fibril formation in vitro , yet how HS impac…
View article: Neuronal<i>Ndst1</i>depletion accelerates prion protein clearance and slows neurodegeneration in prion infection
Neuronal<i>Ndst1</i>depletion accelerates prion protein clearance and slows neurodegeneration in prion infection Open
Select prion diseases are characterized by widespread cerebral plaque-like deposits of amyloid fibrils enriched in heparan sulfate (HS), a major extracellular matrix component. HS facilitates fibril formation in vitro , yet how HS impacts …
View article: Diminished Neuronal ESCRT-0 Function Exacerbates AMPA Receptor Derangement and Accelerates Prion-Induced Neurodegeneration
Diminished Neuronal ESCRT-0 Function Exacerbates AMPA Receptor Derangement and Accelerates Prion-Induced Neurodegeneration Open
Endolysosomal defects in neurons are central to the pathogenesis of prion and other neurodegenerative disorders. In prion disease, prion oligomers traffic through the multivesicular body (MVB) and are routed for degradation in lysosomes or…
View article: Prions induce an early Arc response and a subsequent reduction in mGluR5 in the hippocampus
Prions induce an early Arc response and a subsequent reduction in mGluR5 in the hippocampus Open
Synapse dysfunction and loss are central features of neurodegenerative diseases, caused in part by the accumulation of protein oligomers. Amyloid-β, tau, prion, and α-synuclein oligomers bind to the cellular prion protein (PrPC),
View article: Minimal change prion retinopathy: Morphometric comparison of retinal and brain prion deposits in Creutzfeldt-Jakob disease
Minimal change prion retinopathy: Morphometric comparison of retinal and brain prion deposits in Creutzfeldt-Jakob disease Open
View article: Metabolome Changes during In Vivo Red Cell Aging Reveal Disruption of Key Metabolic Pathways
Metabolome Changes during In Vivo Red Cell Aging Reveal Disruption of Key Metabolic Pathways Open
Understanding the mechanisms for cellular aging is a fundamental question in biology. Normal red blood cells (RBCs) survive for approximately 100 days, and their survival is likely limited by functional decline secondary to cumulative dama…
View article: Prion protein post-translational modifications modulate heparan sulfate binding and limit aggregate size in prion disease
Prion protein post-translational modifications modulate heparan sulfate binding and limit aggregate size in prion disease Open
Many aggregation-prone proteins linked to neurodegenerative disease are post-translationally modified during their biogenesis. In vivo pathogenesis studies have suggested that the presence of post-translational modifications can shift the …
View article: Prion protein glycans reduce intracerebral fibril formation and spongiosis in prion disease
Prion protein glycans reduce intracerebral fibril formation and spongiosis in prion disease Open
Posttranslational modifications (PTMs) are common among proteins that aggregate in neurodegenerative disease, yet how PTMs impact the aggregate conformation and disease progression remains unclear. By engineering knockin mice expressing pr…
View article: Shortening heparan sulfate chains prolongs survival and reduces parenchymal plaques in prion disease caused by mobile, ADAM10-cleaved prions
Shortening heparan sulfate chains prolongs survival and reduces parenchymal plaques in prion disease caused by mobile, ADAM10-cleaved prions Open
View article: Prion Seeds Distribute throughout the Eyes of Sporadic Creutzfeldt-Jakob Disease Patients
Prion Seeds Distribute throughout the Eyes of Sporadic Creutzfeldt-Jakob Disease Patients Open
Cases of iatrogenic prion disease have been reported from corneal transplants, yet the distribution and levels of prions throughout the eye remain unknown. This study probes the occurrence, level, and distribution of prions in the eyes of …
View article: Post-translational modifications in PrP expand the conformational diversity of prions in vivo
Post-translational modifications in PrP expand the conformational diversity of prions in vivo Open