Accumulation of amyloid-β by astrocytes result in enlarged endosomes and microvesicle-induced apoptosis of neurons

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Location: Deutsche Nationalbibliothek Frankfurt am Main

ISSN: 1750-1326

Extent: Online-Ressource

Language: Englisch

Notes: online resource.

Bibliographic citation: Accumulation of amyloid-β by astrocytes result in enlarged endosomes and microvesicle-induced apoptosis of neurons ; volume:11 ; number:1 ; day:12 ; month:5 ; year:2016 ; pages:1-19 ; date:12.2016
Molecular neurodegeneration ; 11, Heft 1 (12.5.2016), 1-19, 12.2016

Creator: Söllvander, Sofia

Contributor: Nikitidou, Elisabeth
Brolin, Robin
Söderberg, Linda
Sehlin, Dag
Lannfelt, Lars
Erlandsson, Anna
SpringerLink (Online service)

DOI: 10.1186/s13024-016-0098-z

URN: urn:nbn:de:1111-2016051726828

Rights: Der Zugriff auf das Objekt ist unbeschränkt möglich.

Last update: 14.08.2025, 10:48 AM CEST

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Söllvander, Sofia
Nikitidou, Elisabeth
Brolin, Robin
Söderberg, Linda
Sehlin, Dag
Lannfelt, Lars
Erlandsson, Anna
SpringerLink (Online service)

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Selective amyloid-β lowering agents

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Accumulation of amyloid-β by astrocytes result in enlarged endosomes and microvesicle-induced apoptosis of neurons

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Other Objects (12)

Amyloid-β accumulation in human astrocytes induces mitochondrial disruption and changed energy metabolism

Origins of amyloid-β

Selective amyloid-β lowering agents

Crosstalk between astrocytes and microglia results in increased degradation of α-synuclein and amyloid-β aggregates

Development of conformation specific Amyloid-β [Amyloid-beta] antibodies

Evidence of amyloid-β cerebral amyloid angiopathy transmission through neurosurgery

The modulating effect of soluble amyloid-β dimers on amyloid-β aggregation in vivo and in vitro

Copper mediated amyloid-β binding to Transthyretin

Hepcidin overexpression in astrocytes alters brain iron metabolism and protects against amyloid-β induced brain damage in mice

Human iPSC-derived astrocytes transplanted into the mouse brain undergo morphological changes in response to amyloid-β plaques

Amyloid-β 1–24 C-terminal truncated fragment promotes amyloid-β 1–42 aggregate formation in the healthy brain

Corynoxine isomers decrease levels of amyloid-β peptide and amyloid-β precursor protein by promoting autophagy and lysosome biogenesis

Amyloid-β accumulation in human astrocytes induces mitochondrial disruption and changed energy metabolism

Origins of amyloid-β

Selective amyloid-β lowering agents

Crosstalk between astrocytes and microglia results in increased degradation of α-synuclein and amyloid-β aggregates

Development of conformation specific Amyloid-β [Amyloid-beta] antibodies

Evidence of amyloid-β cerebral amyloid angiopathy transmission through neurosurgery

The modulating effect of soluble amyloid-β dimers on amyloid-β aggregation in vivo and in vitro

Copper mediated amyloid-β binding to Transthyretin

Hepcidin overexpression in astrocytes alters brain iron metabolism and protects against amyloid-β induced brain damage in mice

Human iPSC-derived astrocytes transplanted into the mouse brain undergo morphological changes in response to amyloid-β plaques

Amyloid-β 1–24 C-terminal truncated fragment promotes amyloid-β 1–42 aggregate formation in the healthy brain

Corynoxine isomers decrease levels of amyloid-β peptide and amyloid-β precursor protein by promoting autophagy and lysosome biogenesis

Amyloid-β accumulation in human astrocytes induces mitochondrial disruption and changed energy metabolism

Origins of amyloid-β

Selective amyloid-β lowering agents

Crosstalk between astrocytes and microglia results in increased degradation of α-synuclein and amyloid-β aggregates

Development of conformation specific Amyloid-β [Amyloid-beta] antibodies

Evidence of amyloid-β cerebral amyloid angiopathy transmission through neurosurgery

The modulating effect of soluble amyloid-β dimers on amyloid-β aggregation in vivo and in vitro

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Hepcidin overexpression in astrocytes alters brain iron metabolism and protects against amyloid-β induced brain damage in mice

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