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Medin aggregation causes cerebrovascular dysfunction in aging wild-type mice

Standard

Medin aggregation causes cerebrovascular dysfunction in aging wild-type mice. / Degenhardt, Karoline; Wagner, Jessica; Skodras, Angelos; Candlish, Michael; Koppelmann, Anna Julia; Wild, Katleen; Maxwell, Rusheka; Rotermund, Carola; von Zweydorf, Felix; Gloeckner, Christian Johannes; Davies, Hannah A; Madine, Jillian; Del Turco, Domenico; Feederle, Regina; Lashley, Tammaryn; Deller, Thomas; Kahle, Philipp; Hefendehl, Jasmin K; Jucker, Mathias; Neher, Jonas J.

in: P NATL ACAD SCI USA, Jahrgang 117, Nr. 38, 22.09.2020, S. 23925-23931.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung

Harvard

Degenhardt, K, Wagner, J, Skodras, A, Candlish, M, Koppelmann, AJ, Wild, K, Maxwell, R, Rotermund, C, von Zweydorf, F, Gloeckner, CJ, Davies, HA, Madine, J, Del Turco, D, Feederle, R, Lashley, T, Deller, T, Kahle, P, Hefendehl, JK, Jucker, M & Neher, JJ 2020, 'Medin aggregation causes cerebrovascular dysfunction in aging wild-type mice', P NATL ACAD SCI USA, Jg. 117, Nr. 38, S. 23925-23931. https://doi.org/10.1073/pnas.2011133117

APA

Degenhardt, K., Wagner, J., Skodras, A., Candlish, M., Koppelmann, A. J., Wild, K., Maxwell, R., Rotermund, C., von Zweydorf, F., Gloeckner, C. J., Davies, H. A., Madine, J., Del Turco, D., Feederle, R., Lashley, T., Deller, T., Kahle, P., Hefendehl, J. K., Jucker, M., & Neher, J. J. (2020). Medin aggregation causes cerebrovascular dysfunction in aging wild-type mice. P NATL ACAD SCI USA, 117(38), 23925-23931. https://doi.org/10.1073/pnas.2011133117

Vancouver

Degenhardt K, Wagner J, Skodras A, Candlish M, Koppelmann AJ, Wild K et al. Medin aggregation causes cerebrovascular dysfunction in aging wild-type mice. P NATL ACAD SCI USA. 2020 Sep 22;117(38):23925-23931. https://doi.org/10.1073/pnas.2011133117

Bibtex

@article{2b6b643919fc4d87970de58240c55cb0,
title = "Medin aggregation causes cerebrovascular dysfunction in aging wild-type mice",
abstract = "Medin is the most common amyloid known in humans, as it can be found in blood vessels of the upper body in virtually everybody over 50 years of age. However, it remains unknown whether deposition of Medin plays a causal role in age-related vascular dysfunction. We now report that aggregates of Medin also develop in the aorta and brain vasculature of wild-type mice in an age-dependent manner. Strikingly, genetic deficiency of the Medin precursor protein, MFG-E8, eliminates not only vascular aggregates but also prevents age-associated decline of cerebrovascular function in mice. Given the prevalence of Medin aggregates in the general population and its role in vascular dysfunction with aging, targeting Medin may become a novel approach to sustain healthy aging.",
keywords = "Aged, 80 and over, Aging/metabolism, Amyloid/genetics, Animals, Antigens, Surface/genetics, Aorta/metabolism, Brain Chemistry/physiology, Cerebrovascular Circulation/physiology, Female, Humans, Male, Mice, Mice, Inbred C57BL, Milk Proteins/genetics, Vascular Diseases/metabolism",
author = "Karoline Degenhardt and Jessica Wagner and Angelos Skodras and Michael Candlish and Koppelmann, {Anna Julia} and Katleen Wild and Rusheka Maxwell and Carola Rotermund and {von Zweydorf}, Felix and Gloeckner, {Christian Johannes} and Davies, {Hannah A} and Jillian Madine and {Del Turco}, Domenico and Regina Feederle and Tammaryn Lashley and Thomas Deller and Philipp Kahle and Hefendehl, {Jasmin K} and Mathias Jucker and Neher, {Jonas J}",
year = "2020",
month = sep,
day = "22",
doi = "10.1073/pnas.2011133117",
language = "English",
volume = "117",
pages = "23925--23931",
journal = "P NATL ACAD SCI USA",
issn = "0027-8424",
publisher = "National Academy of Sciences",
number = "38",

}

RIS

TY - JOUR

T1 - Medin aggregation causes cerebrovascular dysfunction in aging wild-type mice

AU - Degenhardt, Karoline

AU - Wagner, Jessica

AU - Skodras, Angelos

AU - Candlish, Michael

AU - Koppelmann, Anna Julia

AU - Wild, Katleen

AU - Maxwell, Rusheka

AU - Rotermund, Carola

AU - von Zweydorf, Felix

AU - Gloeckner, Christian Johannes

AU - Davies, Hannah A

AU - Madine, Jillian

AU - Del Turco, Domenico

AU - Feederle, Regina

AU - Lashley, Tammaryn

AU - Deller, Thomas

AU - Kahle, Philipp

AU - Hefendehl, Jasmin K

AU - Jucker, Mathias

AU - Neher, Jonas J

PY - 2020/9/22

Y1 - 2020/9/22

N2 - Medin is the most common amyloid known in humans, as it can be found in blood vessels of the upper body in virtually everybody over 50 years of age. However, it remains unknown whether deposition of Medin plays a causal role in age-related vascular dysfunction. We now report that aggregates of Medin also develop in the aorta and brain vasculature of wild-type mice in an age-dependent manner. Strikingly, genetic deficiency of the Medin precursor protein, MFG-E8, eliminates not only vascular aggregates but also prevents age-associated decline of cerebrovascular function in mice. Given the prevalence of Medin aggregates in the general population and its role in vascular dysfunction with aging, targeting Medin may become a novel approach to sustain healthy aging.

AB - Medin is the most common amyloid known in humans, as it can be found in blood vessels of the upper body in virtually everybody over 50 years of age. However, it remains unknown whether deposition of Medin plays a causal role in age-related vascular dysfunction. We now report that aggregates of Medin also develop in the aorta and brain vasculature of wild-type mice in an age-dependent manner. Strikingly, genetic deficiency of the Medin precursor protein, MFG-E8, eliminates not only vascular aggregates but also prevents age-associated decline of cerebrovascular function in mice. Given the prevalence of Medin aggregates in the general population and its role in vascular dysfunction with aging, targeting Medin may become a novel approach to sustain healthy aging.

KW - Aged, 80 and over

KW - Aging/metabolism

KW - Amyloid/genetics

KW - Animals

KW - Antigens, Surface/genetics

KW - Aorta/metabolism

KW - Brain Chemistry/physiology

KW - Cerebrovascular Circulation/physiology

KW - Female

KW - Humans

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Milk Proteins/genetics

KW - Vascular Diseases/metabolism

U2 - 10.1073/pnas.2011133117

DO - 10.1073/pnas.2011133117

M3 - SCORING: Journal article

C2 - 32900929

VL - 117

SP - 23925

EP - 23931

JO - P NATL ACAD SCI USA

JF - P NATL ACAD SCI USA

SN - 0027-8424

IS - 38

ER -