Non-Amyloid-β Component of Human α-Synuclein Oligomers Induces Formation of New Aβ Oligomers: Insight into the Mechanisms That Link Parkinson’s and Alzheimer’s Diseases-Reference-Cited by-同舟云学术

Non-Amyloid-β Component of Human α-Synuclein Oligomers Induces Formation of New Aβ Oligomers: Insight into the Mechanisms That Link Parkinson’s and Alzheimer’s Diseases

Published:2015-10-29 Issue:1 Volume:7 Page:46-55
ISSN:1948-7193
Container-title:ACS Chemical Neuroscience
language:en
Short-container-title:ACS Chem. Neurosci.

Author:

Atsmon-Raz Yoav¹,Miller Yifat¹

Affiliation:

1. Department of Chemistry, ‡Ilse Katz Institute for Nanoscale Science and Technology, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel

Funder

Directorate-General for Research and Innovation

Publisher

American Chemical Society (ACS)

Subject

Cell Biology,Cognitive Neuroscience,Physiology,Biochemistry,General Medicine

Link

https://pubs.acs.org/doi/pdf/10.1021/acschemneuro.5b00204

Reference81 articles.

1. Tau and α-Synuclein Pathology in Amygdala of Parkinsonism-Dementia Complex Patients of Guam

2. Lewy Bodies Contain Altered α-Synuclein in Brains of Many Familial Alzheimer's Disease Patients with Mutations in Presenilin and Amyloid Precursor Protein Genes

3. Antibodies to ?-synuclein detect Lewy bodies in many Down's syndrome brains with Alzheimer's disease

4. Increased amyloid beta-peptide deposition in cerebral cortex as a consequence of apolipoprotein E genotype in late-onset Alzheimer disease.

5. Amyloid-β oligomers: their production, toxicity and therapeutic inhibition

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