Erik C. Gunther
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View article: mGluR4–Npdc1 complex mediates α-synuclein fibril-induced neurodegeneration
mGluR4–Npdc1 complex mediates α-synuclein fibril-induced neurodegeneration Open
Fibrils of misfolded α-synuclein (α-syn) accumulate in Parkinson’s disease and other synucleinopathies, spreading between cells to template further misfolding and drive neurodegeneration. α-syn fibril entry into healthy neurons is recogniz…
View article: Sprinkling in extra validation for high-value PTMs and therapeutic Abs with MILKSHAKE Western blots and Sundae ELISAs
Sprinkling in extra validation for high-value PTMs and therapeutic Abs with MILKSHAKE Western blots and Sundae ELISAs Open
Thoroughly validated antibodies (Abs) are crucial for the generation of meaningful scientific data. Abs for post translationally modified (PTM) protein targets in particular pose added validation challenges. The MILKSHAKE method employs su…
View article: Anti‐PrP<sup>C</sup> antibody rescues cognition and synapses in transgenic alzheimer mice
Anti‐PrP<sup>C</sup> antibody rescues cognition and synapses in transgenic alzheimer mice Open
Objective Amyloid‐beta oligomers (Aßo) trigger the development of Alzheimer's disease ( AD ) pathophysiology. Cellular prion protein (Pr PC ) initiates synaptic damage as a high affinity receptor for Aßo. Here, we evaluated the preclinical…
View article: Rescue of Transgenic Alzheimer’s Pathophysiology by Polymeric Cellular Prion Protein Antagonists
Rescue of Transgenic Alzheimer’s Pathophysiology by Polymeric Cellular Prion Protein Antagonists Open
(Cell Reports 26, 145–158.e1–e8; January 2, 2019) In the originally published version of this article, author name Zahra K. Naderi was misspelled in the author list. This has now been corrected. The authors regret this error. Rescue of Tra…
View article: Rescue of Transgenic Alzheimer’s Pathophysiology by Polymeric Cellular Prion Protein Antagonists
Rescue of Transgenic Alzheimer’s Pathophysiology by Polymeric Cellular Prion Protein Antagonists Open
Cellular prion protein (PrPC) binds the scrapie conformation of PrP (PrPSc) and oligomeric β-amyloid peptide (Aβo) to mediate transmissible spongiform encephalopathy (TSE) and Alzheimer's disease (AD), respectively. W…
View article: Liquid and Hydrogel Phases of PrPC Linked to Conformation Shifts and Triggered by Alzheimer’s Amyloid-β Oligomers
Liquid and Hydrogel Phases of PrPC Linked to Conformation Shifts and Triggered by Alzheimer’s Amyloid-β Oligomers Open
View article: NMR Data for Liquid and Hydrogel Phases of PrPC Linked to Conformation Shifts and Triggered by Alzheimer’s Amyloid-β Oligomers
NMR Data for Liquid and Hydrogel Phases of PrPC Linked to Conformation Shifts and Triggered by Alzheimer’s Amyloid-β Oligomers Open
1D and 2D multidimensional solution and solid-state NMR spectroscopy date for PrP and Abo phase separation and hydrogel formation. For 1D data, files are frequency domain XY data in comma separated format, with column 1 being the chemical …
View article: Prion-Protein-interacting Amyloid-β Oligomers of High Molecular Weight Are Tightly Correlated with Memory Impairment in Multiple Alzheimer Mouse Models
Prion-Protein-interacting Amyloid-β Oligomers of High Molecular Weight Are Tightly Correlated with Memory Impairment in Multiple Alzheimer Mouse Models Open
Alzheimer disease (AD) is characterized by amyloid-β accumulation, with soluble oligomers (Aβo) being the most synaptotoxic. However, the multivalent and unstable nature of Aβo limits molecular characterization and hinders research reprodu…
View article: <scp>F</scp>yn inhibition rescues established memory and synapse loss in <scp>A</scp>lzheimer mice
<span>F</span>yn inhibition rescues established memory and synapse loss in <span>A</span>lzheimer mice Open
Objective Currently no effective disease‐modifying agents exist for the treatment of Alzheimer disease (AD). The Fyn tyrosine kinase is implicated in AD pathology triggered by amyloid‐ß oligomers (Aßo) and propagated by Tau. Thus, Fyn inhi…