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β2-Microglobulin boosts β-amyloid aggregation and neurotoxicity in an Alzheimer’s disease model
in
631/378/1689/1283
/ 692/699/375/132/1283
/ Alzheimer Disease
/ Alzheimer's disease
/ Amyloid
/ Amyloid beta-Peptides
/ Amyloidogenesis
/ Animal Genetics and Genomics
/ Behavioral Sciences
/ Biological Techniques
/ Biomedical and Life Sciences
/ Biomedicine
/ Cognitive ability
/ Humans
/ Neurobiology
/ Neurodegenerative diseases
/ Neurosciences
/ Neurotoxicity
/ Neutralization
/ Research Briefing
/ β-Amyloid
/ β2 Microglobulin
2023
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β2-Microglobulin boosts β-amyloid aggregation and neurotoxicity in an Alzheimer’s disease model
by
in
631/378/1689/1283
/ 692/699/375/132/1283
/ Alzheimer Disease
/ Alzheimer's disease
/ Amyloid
/ Amyloid beta-Peptides
/ Amyloidogenesis
/ Animal Genetics and Genomics
/ Behavioral Sciences
/ Biological Techniques
/ Biomedical and Life Sciences
/ Biomedicine
/ Cognitive ability
/ Humans
/ Neurobiology
/ Neurodegenerative diseases
/ Neurosciences
/ Neurotoxicity
/ Neutralization
/ Research Briefing
/ β-Amyloid
/ β2 Microglobulin
2023
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Do you wish to request the book?
β2-Microglobulin boosts β-amyloid aggregation and neurotoxicity in an Alzheimer’s disease model
in
631/378/1689/1283
/ 692/699/375/132/1283
/ Alzheimer Disease
/ Alzheimer's disease
/ Amyloid
/ Amyloid beta-Peptides
/ Amyloidogenesis
/ Animal Genetics and Genomics
/ Behavioral Sciences
/ Biological Techniques
/ Biomedical and Life Sciences
/ Biomedicine
/ Cognitive ability
/ Humans
/ Neurobiology
/ Neurodegenerative diseases
/ Neurosciences
/ Neurotoxicity
/ Neutralization
/ Research Briefing
/ β-Amyloid
/ β2 Microglobulin
2023
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β2-Microglobulin boosts β-amyloid aggregation and neurotoxicity in an Alzheimer’s disease model
Journal Article
β2-Microglobulin boosts β-amyloid aggregation and neurotoxicity in an Alzheimer’s disease model
2023
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Overview
β2-Microglobulin (β
2
M) is an amyloidogenic protein. β
2
M coaggregates with β-amyloid (Aβ) in the brains of patients with Alzheimer’s disease and enhances Aβ deposition. β
2
M is essential for Aβ neurotoxicity in vivo, and neutralization of pathogenetic β
2
M–Aβ aggregates ameliorates the amyloid pathology and cognitive deficits associated with disease in a mouse model.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
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