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

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Abstract: Alzheimer's Disease (AD) is a neurodegenerative condition characterized by the accumulation and deposition of amyloid‐β (Aβ) aggregates in the brain. Despite a wealth of research on the toxicity of Aβ and its role in synaptic damage, the mechanisms facilitating Aβ clearance are not yet fully understood. However, microglia, the primary immune cells of the central nervous system, are known to maintain homeostasis through the phagocytic clearance of protein aggregates and cellular debris. In this study, RNA sequencing analysis and live cell functional screens are employed to uncover microglial genetic modifiers related to AD. Lyzl4 is identified, which encodes a c‐type lysozyme‐like enzyme primarily localized to microglial lysosomes, as a gene significantly upregulated in AD microglia with aging and propose that Lyzl4 upregulation acts as a positive regulator of Aβ clearance. Furthermore, it is found that Lyzl4 overexpression boosts Aβ clearance both in vitro and in vivo, underscoring its potential for mitigating Aβ burden. These novel insights position Lyzl4 as a promising therapeutic target for Alzheimer's disease, paving the way for further exploration into potential AD treatments.

Location: Deutsche Nationalbibliothek Frankfurt am Main

Extent: Online-Ressource

Language: Englisch

Bibliographic citation: Microglial Lyzl4 Facilitates β‐Amyloid Clearance in Alzheimer's Disease ; day:18 ; month:11 ; year:2024 ; extent:12
Advanced science ; (18.11.2024) (gesamt 12)

Creator: Pan, Jie
Zhong, Jie
Geng, Ji
Oberhauser, Jane
Shi, Shihua
Wan, Jun

DOI: 10.1002/advs.202412184

URN: urn:nbn:de:101:1-2411181337107.823955533622

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

Last update: 15.08.2025, 7:33 AM CEST

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Pan, Jie
Zhong, Jie
Geng, Ji
Oberhauser, Jane
Shi, Shihua
Wan, Jun

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Hochschulschrift

Selektion hochaffiner RNA-Moleküle gegen das Alzheimer β-Amyloid [Beta-Amyloid]

Hochschulschrift

Selektion hochaffiner RNA-Moleküle gegen das Alzheimer β-Amyloid [Beta-Amyloid]

Microglial phagocytosis induced by fibrillar β-amyloid is attenuated by oligomeric β-amyloid: implications for Alzheimer's disease

Microglial amyloid beta clearance is driven by PIEZO1 channels

Microglial MAC1 receptor and PI3K are essential in mediating β-amyloid peptide-induced microglial activation and subsequent neurotoxicity

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

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

Accumulated BCAAs and BCKAs contribute to the HFD-induced deterioration of Alzheimer's disease via a dysfunctional TREM2-related reduction in microglial β-amyloid clearance

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

The mixed-lineage kinase 3 inhibitor URMC-099 facilitates microglial amyloid-β degradation

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Fully automated and highly specific plasma β-amyloid immunoassays predict β-amyloid status defined by amyloid positron emission tomography with high accuracy

Hochschulschrift

Selektion hochaffiner RNA-Moleküle gegen das Alzheimer β-Amyloid [Beta-Amyloid]

Hochschulschrift

Selektion hochaffiner RNA-Moleküle gegen das Alzheimer β-Amyloid [Beta-Amyloid]

Microglial phagocytosis induced by fibrillar β-amyloid is attenuated by oligomeric β-amyloid: implications for Alzheimer's disease

Microglial amyloid beta clearance is driven by PIEZO1 channels

Microglial MAC1 receptor and PI3K are essential in mediating β-amyloid peptide-induced microglial activation and subsequent neurotoxicity

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

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

Accumulated BCAAs and BCKAs contribute to the HFD-induced deterioration of Alzheimer's disease via a dysfunctional TREM2-related reduction in microglial β-amyloid clearance

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

The mixed-lineage kinase 3 inhibitor URMC-099 facilitates microglial amyloid-β degradation

Cudrania cochinchinensis attenuates amyloid β protein-mediated microglial activation and promotes glia-related clearance of amyloid β protein

Fully automated and highly specific plasma β-amyloid immunoassays predict β-amyloid status defined by amyloid positron emission tomography with high accuracy

Hochschulschrift

Selektion hochaffiner RNA-Moleküle gegen das Alzheimer β-Amyloid [Beta-Amyloid]

Hochschulschrift

Selektion hochaffiner RNA-Moleküle gegen das Alzheimer β-Amyloid [Beta-Amyloid]

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

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Other Objects (12)

Microglial phagocytosis induced by fibrillar β-amyloid is attenuated by oligomeric β-amyloid: implications for Alzheimer's disease

Microglial amyloid beta clearance is driven by PIEZO1 channels

Microglial MAC1 receptor and PI3K are essential in mediating β-amyloid peptide-induced microglial activation and subsequent neurotoxicity

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

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

Accumulated BCAAs and BCKAs contribute to the HFD-induced deterioration of Alzheimer's disease via a dysfunctional TREM2-related reduction in microglial β-amyloid clearance

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

The mixed-lineage kinase 3 inhibitor URMC-099 facilitates microglial amyloid-β degradation

Cudrania cochinchinensis attenuates amyloid β protein-mediated microglial activation and promotes glia-related clearance of amyloid β protein

Fully automated and highly specific plasma β-amyloid immunoassays predict β-amyloid status defined by amyloid positron emission tomography with high accuracy

Selektion hochaffiner RNA-Moleküle gegen das Alzheimer β-Amyloid [Beta-Amyloid]

Selektion hochaffiner RNA-Moleküle gegen das Alzheimer β-Amyloid [Beta-Amyloid]

Microglial phagocytosis induced by fibrillar β-amyloid is attenuated by oligomeric β-amyloid: implications for Alzheimer's disease

Microglial amyloid beta clearance is driven by PIEZO1 channels

Microglial MAC1 receptor and PI3K are essential in mediating β-amyloid peptide-induced microglial activation and subsequent neurotoxicity

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

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

Accumulated BCAAs and BCKAs contribute to the HFD-induced deterioration of Alzheimer's disease via a dysfunctional TREM2-related reduction in microglial β-amyloid clearance

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

The mixed-lineage kinase 3 inhibitor URMC-099 facilitates microglial amyloid-β degradation

Cudrania cochinchinensis attenuates amyloid β protein-mediated microglial activation and promotes glia-related clearance of amyloid β protein

Fully automated and highly specific plasma β-amyloid immunoassays predict β-amyloid status defined by amyloid positron emission tomography with high accuracy

Selektion hochaffiner RNA-Moleküle gegen das Alzheimer β-Amyloid [Beta-Amyloid]

Selektion hochaffiner RNA-Moleküle gegen das Alzheimer β-Amyloid [Beta-Amyloid]

Microglial phagocytosis induced by fibrillar β-amyloid is attenuated by oligomeric β-amyloid: implications for Alzheimer's disease

Microglial amyloid beta clearance is driven by PIEZO1 channels

Microglial MAC1 receptor and PI3K are essential in mediating β-amyloid peptide-induced microglial activation and subsequent neurotoxicity

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

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

Accumulated BCAAs and BCKAs contribute to the HFD-induced deterioration of Alzheimer's disease via a dysfunctional TREM2-related reduction in microglial β-amyloid clearance

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

The mixed-lineage kinase 3 inhibitor URMC-099 facilitates microglial amyloid-β degradation

Cudrania cochinchinensis attenuates amyloid β protein-mediated microglial activation and promotes glia-related clearance of amyloid β protein

Fully automated and highly specific plasma β-amyloid immunoassays predict β-amyloid status defined by amyloid positron emission tomography with high accuracy

Selektion hochaffiner RNA-Moleküle gegen das Alzheimer β-Amyloid [Beta-Amyloid]

Selektion hochaffiner RNA-Moleküle gegen das Alzheimer β-Amyloid [Beta-Amyloid]

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