Adropin correlates with aging-related neuropathology in humans and improves cognitive function in aging mice

Abstract The neural functions of adropin, a secreted peptide highly expressed in the brain, have not been investigated. In humans, adropin is highly expressed in astrocytes and peaks during critical postnatal periods of brain development. Gene enrichment analysis of transcripts correlating with adro...

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Autores principales:	Subhashis Banerjee, Sarbani Ghoshal, Clemence Girardet, Kelly M. DeMars, Changjun Yang, Michael L. Niehoff, Andrew D. Nguyen, Prerana Jayanth, Brittany A. Hoelscher, Fenglian Xu, William A. Banks, Kim M. Hansen, Jinsong Zhang, Eduardo Candelario-Jalil, Susan A. Farr, Andrew A. Butler
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Geriatrics RC952-954.6
Acceso en línea:	https://doaj.org/article/76f1c0c442654891acc905cc4c82ecdb
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spelling	oai:doaj.org-article:76f1c0c442654891acc905cc4c82ecdb2021-12-02T19:04:25ZAdropin correlates with aging-related neuropathology in humans and improves cognitive function in aging mice10.1038/s41514-021-00076-52056-3973https://doaj.org/article/76f1c0c442654891acc905cc4c82ecdb2021-08-01T00:00:00Zhttps://doi.org/10.1038/s41514-021-00076-5https://doaj.org/toc/2056-3973Abstract The neural functions of adropin, a secreted peptide highly expressed in the brain, have not been investigated. In humans, adropin is highly expressed in astrocytes and peaks during critical postnatal periods of brain development. Gene enrichment analysis of transcripts correlating with adropin expression suggests processes relevant to aging-related neurodegenerative diseases that vary with age and dementia state, possibly indicating survivor bias. In people aged <40 y and ‘old-old’ (>75 y) diagnosed with dementia, adropin correlates positively with genes involved in mitochondrial processes. In the ‘old-old’ without dementia adropin expression correlates positively with morphogenesis and synapse function. Potent neurotrophic responses in primary cultured neurons are consistent with adropin supporting the development and function of neural networks. Adropin expression in the ‘old-old’ also correlates positively with protein markers of tau-related neuropathologies and inflammation, particularly in those without dementia. How variation in brain adropin expression affects neurological aging was investigated using old (18-month) C57BL/6J mice. In mice adropin is expressed in neurons, oligodendrocyte progenitor cells, oligodendrocytes, and microglia and shows correlative relationships with groups of genes involved in neurodegeneration and cellular metabolism. Increasing adropin expression using transgenesis improved spatial learning and memory, novel object recognition, resilience to exposure to new environments, and reduced mRNA markers of inflammation in old mice. Treatment with synthetic adropin peptide also reversed age-related declines in cognitive functions and affected expression of genes involved in morphogenesis and cellular metabolism. Collectively, these results establish a link between adropin expression and neural energy metabolism and indicate a potential therapy against neurological aging.Subhashis BanerjeeSarbani GhoshalClemence GirardetKelly M. DeMarsChangjun YangMichael L. NiehoffAndrew D. NguyenPrerana JayanthBrittany A. HoelscherFenglian XuWilliam A. BanksKim M. HansenJinsong ZhangEduardo Candelario-JalilSusan A. FarrAndrew A. ButlerNature PortfolioarticleGeriatricsRC952-954.6ENnpj Aging and Mechanisms of Disease, Vol 7, Iss 1, Pp 1-17 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Geriatrics RC952-954.6
spellingShingle	Geriatrics RC952-954.6 Subhashis Banerjee Sarbani Ghoshal Clemence Girardet Kelly M. DeMars Changjun Yang Michael L. Niehoff Andrew D. Nguyen Prerana Jayanth Brittany A. Hoelscher Fenglian Xu William A. Banks Kim M. Hansen Jinsong Zhang Eduardo Candelario-Jalil Susan A. Farr Andrew A. Butler Adropin correlates with aging-related neuropathology in humans and improves cognitive function in aging mice
description	Abstract The neural functions of adropin, a secreted peptide highly expressed in the brain, have not been investigated. In humans, adropin is highly expressed in astrocytes and peaks during critical postnatal periods of brain development. Gene enrichment analysis of transcripts correlating with adropin expression suggests processes relevant to aging-related neurodegenerative diseases that vary with age and dementia state, possibly indicating survivor bias. In people aged <40 y and ‘old-old’ (>75 y) diagnosed with dementia, adropin correlates positively with genes involved in mitochondrial processes. In the ‘old-old’ without dementia adropin expression correlates positively with morphogenesis and synapse function. Potent neurotrophic responses in primary cultured neurons are consistent with adropin supporting the development and function of neural networks. Adropin expression in the ‘old-old’ also correlates positively with protein markers of tau-related neuropathologies and inflammation, particularly in those without dementia. How variation in brain adropin expression affects neurological aging was investigated using old (18-month) C57BL/6J mice. In mice adropin is expressed in neurons, oligodendrocyte progenitor cells, oligodendrocytes, and microglia and shows correlative relationships with groups of genes involved in neurodegeneration and cellular metabolism. Increasing adropin expression using transgenesis improved spatial learning and memory, novel object recognition, resilience to exposure to new environments, and reduced mRNA markers of inflammation in old mice. Treatment with synthetic adropin peptide also reversed age-related declines in cognitive functions and affected expression of genes involved in morphogenesis and cellular metabolism. Collectively, these results establish a link between adropin expression and neural energy metabolism and indicate a potential therapy against neurological aging.
format	article
author	Subhashis Banerjee Sarbani Ghoshal Clemence Girardet Kelly M. DeMars Changjun Yang Michael L. Niehoff Andrew D. Nguyen Prerana Jayanth Brittany A. Hoelscher Fenglian Xu William A. Banks Kim M. Hansen Jinsong Zhang Eduardo Candelario-Jalil Susan A. Farr Andrew A. Butler
author_facet	Subhashis Banerjee Sarbani Ghoshal Clemence Girardet Kelly M. DeMars Changjun Yang Michael L. Niehoff Andrew D. Nguyen Prerana Jayanth Brittany A. Hoelscher Fenglian Xu William A. Banks Kim M. Hansen Jinsong Zhang Eduardo Candelario-Jalil Susan A. Farr Andrew A. Butler
author_sort	Subhashis Banerjee
title	Adropin correlates with aging-related neuropathology in humans and improves cognitive function in aging mice
title_short	Adropin correlates with aging-related neuropathology in humans and improves cognitive function in aging mice
title_full	Adropin correlates with aging-related neuropathology in humans and improves cognitive function in aging mice
title_fullStr	Adropin correlates with aging-related neuropathology in humans and improves cognitive function in aging mice
title_full_unstemmed	Adropin correlates with aging-related neuropathology in humans and improves cognitive function in aging mice
title_sort	adropin correlates with aging-related neuropathology in humans and improves cognitive function in aging mice
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/76f1c0c442654891acc905cc4c82ecdb
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Adropin correlates with aging-related neuropathology in humans and improves cognitive function in aging mice

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