date: 2022-11-08T06:43:33Z
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pdf:docinfo:title: The Hidden Role of Non-Canonical Amyloid  Isoforms in Alzheimer?s Disease
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Keywords: Amyloid Beta; Alzheimer?s Disease; APP; neuroinflammation; glia; microglia; neurodegeneration; cell-surface receptors
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subject: Recent advances have placed the pro-inflammatory activity of amyloid  (A) on microglia cells as the focus of research on Alzheimer?s Disease (AD). Researchers are confronted with an astonishing spectrum of over 100 different A variants with variable length and chemical modifications. With the exception of A1-42 and A1-40, the biological significance of most peptides for AD is as yet insufficiently understood. We therefore aim to provide a comprehensive overview of the contributions of these neglected A variants to microglia activation. First, the impact of A receptors, signaling cascades, scavenger mechanisms, and genetic variations on the physiological responses towards various A species is described. Furthermore, we discuss the importance of different types of amyloid precursor protein processing for the generation of these A variants in microglia, astrocytes, oligodendrocytes, and neurons, and highlight how alterations in secondary structures and oligomerization affect A neurotoxicity. In sum, the data indicate that gene polymorphisms in A-driven signaling pathways in combination with the production and activity of different A variants might be crucial factors for the initiation and progression of different forms of AD. A deeper assessment of their interplay with glial cells may pave the way towards novel therapeutic strategies for individualized medicine.
dc:creator: Lukas Busch, Simone Eggert, Kristina Endres and Bernd Bufe
dcterms:created: 2022-11-08T05:51:38Z
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title: The Hidden Role of Non-Canonical Amyloid  Isoforms in Alzheimer?s Disease
Last-Save-Date: 2022-11-08T06:43:33Z
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pdf:docinfo:keywords: Amyloid Beta; Alzheimer?s Disease; APP; neuroinflammation; glia; microglia; neurodegeneration; cell-surface receptors
pdf:docinfo:modified: 2022-11-08T06:43:33Z
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dc:title: The Hidden Role of Non-Canonical Amyloid  Isoforms in Alzheimer?s Disease
modified: 2022-11-08T06:43:33Z
cp:subject: Recent advances have placed the pro-inflammatory activity of amyloid  (A) on microglia cells as the focus of research on Alzheimer?s Disease (AD). Researchers are confronted with an astonishing spectrum of over 100 different A variants with variable length and chemical modifications. With the exception of A1-42 and A1-40, the biological significance of most peptides for AD is as yet insufficiently understood. We therefore aim to provide a comprehensive overview of the contributions of these neglected A variants to microglia activation. First, the impact of A receptors, signaling cascades, scavenger mechanisms, and genetic variations on the physiological responses towards various A species is described. Furthermore, we discuss the importance of different types of amyloid precursor protein processing for the generation of these A variants in microglia, astrocytes, oligodendrocytes, and neurons, and highlight how alterations in secondary structures and oligomerization affect A neurotoxicity. In sum, the data indicate that gene polymorphisms in A-driven signaling pathways in combination with the production and activity of different A variants might be crucial factors for the initiation and progression of different forms of AD. A deeper assessment of their interplay with glial cells may pave the way towards novel therapeutic strategies for individualized medicine.
pdf:docinfo:subject: Recent advances have placed the pro-inflammatory activity of amyloid  (A) on microglia cells as the focus of research on Alzheimer?s Disease (AD). Researchers are confronted with an astonishing spectrum of over 100 different A variants with variable length and chemical modifications. With the exception of A1-42 and A1-40, the biological significance of most peptides for AD is as yet insufficiently understood. We therefore aim to provide a comprehensive overview of the contributions of these neglected A variants to microglia activation. First, the impact of A receptors, signaling cascades, scavenger mechanisms, and genetic variations on the physiological responses towards various A species is described. Furthermore, we discuss the importance of different types of amyloid precursor protein processing for the generation of these A variants in microglia, astrocytes, oligodendrocytes, and neurons, and highlight how alterations in secondary structures and oligomerization affect A neurotoxicity. In sum, the data indicate that gene polymorphisms in A-driven signaling pathways in combination with the production and activity of different A variants might be crucial factors for the initiation and progression of different forms of AD. A deeper assessment of their interplay with glial cells may pave the way towards novel therapeutic strategies for individualized medicine.
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pdf:docinfo:creator: Lukas Busch, Simone Eggert, Kristina Endres and Bernd Bufe
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creator: Lukas Busch, Simone Eggert, Kristina Endres and Bernd Bufe
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dc:subject: Amyloid Beta; Alzheimer?s Disease; APP; neuroinflammation; glia; microglia; neurodegeneration; cell-surface receptors
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meta:keyword: Amyloid Beta; Alzheimer?s Disease; APP; neuroinflammation; glia; microglia; neurodegeneration; cell-surface receptors
Author: Lukas Busch, Simone Eggert, Kristina Endres and Bernd Bufe
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