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Einar M. Sigurdsson

Researcher at New York University

Publications -  140
Citations -  13502

Einar M. Sigurdsson is an academic researcher from New York University. The author has contributed to research in topics: Tau protein & Tauopathy. The author has an hindex of 45, co-authored 134 publications receiving 12236 citations. Previous affiliations of Einar M. Sigurdsson include York University & Loyola University Chicago.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Beta-sheet breaker peptides inhibit fibrillogenesis in a rat brain model of amyloidosis: implications for Alzheimer's therapy.

TL;DR: A 5-residue peptide is demonstrated that inhibits amyloid βprotein fibrillogenesis, disassembles preformed fibrils in vitro and prevents neuronal death induced by fibrILS in cell culture and may provide the basis for a new therapeutic approach to prevent amyloidsosis in Alzheimer's disease.
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Tau-targeting therapies for Alzheimer disease.

TL;DR: Therapies for Alzheimer disease in clinical trials are gradually shifting from amyloid-β (Aβ)-targeting to tau-targeting approaches, and tau is likely to be a better target than Aβ once cognitive deficits manifest because the tau burden correlates better with clinical impairments than does the Aβ burden.
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Immunotherapy Targeting Pathological Tau Conformers in a Tangle Mouse Model Reduces Brain Pathology with Associated Functional Improvements

TL;DR: It is presented that active immunization with a phosphorylated tau epitope, in P301L tangle model mice, reduces aggregated tau in the brain and slows progression of the tangle-related behavioral phenotype and may lead to a novel therapy targeting one of the major hallmarks of Alzheimer's disease and frontotemporal dementia.
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Immunization with a Nontoxic/Nonfibrillar Amyloid-β Homologous Peptide Reduces Alzheimer's Disease-Associated Pathology in Transgenic Mice

TL;DR: It is reported that immunization in transgenic APP mice for 7 months with a soluble nonamyloidogenic, nontoxic Abeta homologous peptide reduced cortical and hippocampal brain amyloid burden and brain levels of soluble Abeta1-42 were reduced, indicating reduced inflammation in these animals.