Gender-specific relationship between thigh muscle and fat mass and brain amyloid-β positivity

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Location: Deutsche Nationalbibliothek Frankfurt am Main

ISSN: 1758-9193

Extent: Online-Ressource

Language: Englisch

Notes: online resource.

Bibliographic citation: Gender-specific relationship between thigh muscle and fat mass and brain amyloid-β positivity ; volume:14 ; number:1 ; day:4 ; month:10 ; year:2022 ; pages:1-9 ; date:12.2022
Alzheimer's research & therapy ; 14, Heft 1 (4.10.2022), 1-9, 12.2022

Creator: Kang, Sung Hoon
Lee, Kyung Hyun
Chang, Yoosoo
Choe, Yeong Sim
Kim, Jun Pyo
Jang, Hyemin
Shin, Hee Young
Kim, Hee Jin
Koh, Seong-Beom
Na, Duk L.
Seo, Sang Won
Kang, Mira

Contributor: SpringerLink (Online service)

DOI: 10.1186/s13195-022-01086-5

URN: urn:nbn:de:101:1-2022122409401814045966

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

Last update: 15.08.2025, 7:26 AM CEST

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Associated

Kang, Sung Hoon
Lee, Kyung Hyun
Chang, Yoosoo
Choe, Yeong Sim
Kim, Jun Pyo
Jang, Hyemin
Shin, Hee Young
Kim, Hee Jin
Koh, Seong-Beom
Na, Duk L.
Seo, Sang Won
Kang, Mira
SpringerLink (Online service)

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Gender-specific relationship between thigh muscle and fat mass and brain amyloid-β positivity

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Other Objects (12)

Characteristics of discordance between amyloid positron emission tomography and plasma amyloid-β 42/40 positivity

Origins of amyloid-β

Longitudinal pathways of cerebrospinal fluid and positron emission tomography biomarkers of amyloid-β positivity

Prediction of amyloid PET positivity via machine learning algorithms trained with EDTA-based blood amyloid-β oligomerization data

Selective amyloid-β lowering agents

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

Comparative Analysis of Different Definitions of Amyloid-β Positivity to Detect Early Downstream Pathophysiological Alterations in Preclinical Alzheimer

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

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

Characteristics of discordance between amyloid positron emission tomography and plasma amyloid-β 42/40 positivity

Origins of amyloid-β

Longitudinal pathways of cerebrospinal fluid and positron emission tomography biomarkers of amyloid-β positivity

Prediction of amyloid PET positivity via machine learning algorithms trained with EDTA-based blood amyloid-β oligomerization data

Selective amyloid-β lowering agents

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

Comparative Analysis of Different Definitions of Amyloid-β Positivity to Detect Early Downstream Pathophysiological Alterations in Preclinical Alzheimer

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

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

Characteristics of discordance between amyloid positron emission tomography and plasma amyloid-β 42/40 positivity

Origins of amyloid-β

Longitudinal pathways of cerebrospinal fluid and positron emission tomography biomarkers of amyloid-β positivity

Prediction of amyloid PET positivity via machine learning algorithms trained with EDTA-based blood amyloid-β oligomerization data

Selective amyloid-β lowering agents

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

Comparative Analysis of Different Definitions of Amyloid-β Positivity to Detect Early Downstream Pathophysiological Alterations in Preclinical Alzheimer

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