BACE1 regulates expression of Clusterin in astrocytes for enhancing clearance of β-amyloid peptides

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Location: Deutsche Nationalbibliothek Frankfurt am Main

Extent: Online-Ressource, 1 online resource.

Language: Englisch

Bibliographic citation: BACE1 regulates expression of Clusterin in astrocytes for enhancing clearance of β-amyloid peptides ; volume:18 ; number:1 ; day:4 ; month:5 ; year:2023 ; pages:1-20 ; date:12.2023
Molecular neurodegeneration ; 18, Heft 1 (4.5.2023), 1-20, 12.2023

Creator: Zhou, John
Singh, Neeraj
Galske, James
Hudobenko, Jacob
Hu, Xiangyou
Yan, Riqiang

Contributor: SpringerLink (Online service)

DOI: 10.1186/s13024-023-00611-w

URN: urn:nbn:de:101:1-2023090608503922415580

Rights: Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.

Last update: 14.08.2025, 10:58 AM CEST

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Zhou, John
Singh, Neeraj
Galske, James
Hudobenko, Jacob
Hu, Xiangyou
Yan, Riqiang
SpringerLink (Online service)

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BACE1 inhibition more effectively suppresses initiation than progression of β-amyloid pathology

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Pharmacological BACE1 inhibitor treatment during early progression of β-amyloid pathology maximizes therapeutic efficacy

Chronic Toxoplasma gondii infection enhances β-amyloid phagocytosis and clearance by recruited monocytes

Brain clearance of protein aggregates: a close-up on astrocytes

Non-neuronal and neuronal BACE1 elevation in association with angiopathic and leptomeningeal β-amyloid deposition in the human brain

β-Amyloid promotes accumulation of lipid peroxides by inhibiting CD36-mediated clearance of oxidized lipoproteins

Sorting nexin 12 interacts with BACE1 and regulates BACE1-mediated APP processing

Aβ34 is a BACE1-derived degradation intermediate associated with amyloid clearance and Alzheimer’s disease progression

BACE1 is at the crossroad of a toxic vicious cycle involving cellular stress and β-amyloid production in Alzheimer’s disease

BACE1 elevation engendered by GGA3 deletion increases β-amyloid pathology in association with APP elevation and decreased CHL1 processing in 5XFAD mice

The effect of BACE1-AS on β-amyloid generation by regulating BACE1 mRNA expression

BACE1 inhibition more effectively suppresses initiation than progression of β-amyloid pathology

Microglial Lyzl4 Facilitates β‐Amyloid Clearance in Alzheimer's Disease

Pharmacological BACE1 inhibitor treatment during early progression of β-amyloid pathology maximizes therapeutic efficacy

Chronic Toxoplasma gondii infection enhances β-amyloid phagocytosis and clearance by recruited monocytes

Brain clearance of protein aggregates: a close-up on astrocytes

Non-neuronal and neuronal BACE1 elevation in association with angiopathic and leptomeningeal β-amyloid deposition in the human brain

β-Amyloid promotes accumulation of lipid peroxides by inhibiting CD36-mediated clearance of oxidized lipoproteins

Sorting nexin 12 interacts with BACE1 and regulates BACE1-mediated APP processing

Aβ34 is a BACE1-derived degradation intermediate associated with amyloid clearance and Alzheimer’s disease progression

BACE1 is at the crossroad of a toxic vicious cycle involving cellular stress and β-amyloid production in Alzheimer’s disease

BACE1 elevation engendered by GGA3 deletion increases β-amyloid pathology in association with APP elevation and decreased CHL1 processing in 5XFAD mice

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BACE1 regulates expression of Clusterin in astrocytes for enhancing clearance of β-amyloid peptides

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Other Objects (12)

The effect of BACE1-AS on β-amyloid generation by regulating BACE1 mRNA expression

BACE1 inhibition more effectively suppresses initiation than progression of β-amyloid pathology

Microglial Lyzl4 Facilitates β‐Amyloid Clearance in Alzheimer's Disease

Pharmacological BACE1 inhibitor treatment during early progression of β-amyloid pathology maximizes therapeutic efficacy

Chronic Toxoplasma gondii infection enhances β-amyloid phagocytosis and clearance by recruited monocytes

Brain clearance of protein aggregates: a close-up on astrocytes

Non-neuronal and neuronal BACE1 elevation in association with angiopathic and leptomeningeal β-amyloid deposition in the human brain

β-Amyloid promotes accumulation of lipid peroxides by inhibiting CD36-mediated clearance of oxidized lipoproteins

Sorting nexin 12 interacts with BACE1 and regulates BACE1-mediated APP processing

Aβ34 is a BACE1-derived degradation intermediate associated with amyloid clearance and Alzheimer’s disease progression

BACE1 is at the crossroad of a toxic vicious cycle involving cellular stress and β-amyloid production in Alzheimer’s disease

BACE1 elevation engendered by GGA3 deletion increases β-amyloid pathology in association with APP elevation and decreased CHL1 processing in 5XFAD mice

The effect of BACE1-AS on β-amyloid generation by regulating BACE1 mRNA expression

BACE1 inhibition more effectively suppresses initiation than progression of β-amyloid pathology

Microglial Lyzl4 Facilitates β‐Amyloid Clearance in Alzheimer's Disease

Pharmacological BACE1 inhibitor treatment during early progression of β-amyloid pathology maximizes therapeutic efficacy

Chronic Toxoplasma gondii infection enhances β-amyloid phagocytosis and clearance by recruited monocytes

Brain clearance of protein aggregates: a close-up on astrocytes

Non-neuronal and neuronal BACE1 elevation in association with angiopathic and leptomeningeal β-amyloid deposition in the human brain

β-Amyloid promotes accumulation of lipid peroxides by inhibiting CD36-mediated clearance of oxidized lipoproteins

Sorting nexin 12 interacts with BACE1 and regulates BACE1-mediated APP processing

Aβ34 is a BACE1-derived degradation intermediate associated with amyloid clearance and Alzheimer’s disease progression

BACE1 is at the crossroad of a toxic vicious cycle involving cellular stress and β-amyloid production in Alzheimer’s disease

BACE1 elevation engendered by GGA3 deletion increases β-amyloid pathology in association with APP elevation and decreased CHL1 processing in 5XFAD mice

The effect of BACE1-AS on β-amyloid generation by regulating BACE1 mRNA expression

BACE1 inhibition more effectively suppresses initiation than progression of β-amyloid pathology

Microglial Lyzl4 Facilitates β‐Amyloid Clearance in Alzheimer's Disease

Pharmacological BACE1 inhibitor treatment during early progression of β-amyloid pathology maximizes therapeutic efficacy

Chronic Toxoplasma gondii infection enhances β-amyloid phagocytosis and clearance by recruited monocytes

Brain clearance of protein aggregates: a close-up on astrocytes

Non-neuronal and neuronal BACE1 elevation in association with angiopathic and leptomeningeal β-amyloid deposition in the human brain

β-Amyloid promotes accumulation of lipid peroxides by inhibiting CD36-mediated clearance of oxidized lipoproteins

Sorting nexin 12 interacts with BACE1 and regulates BACE1-mediated APP processing

Aβ34 is a BACE1-derived degradation intermediate associated with amyloid clearance and Alzheimer’s disease progression

BACE1 is at the crossroad of a toxic vicious cycle involving cellular stress and β-amyloid production in Alzheimer’s disease

BACE1 elevation engendered by GGA3 deletion increases β-amyloid pathology in association with APP elevation and decreased CHL1 processing in 5XFAD mice

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