Localization of endogenous amyloid-β to the coeruleo-cortical pathway: consequences of noradrenergic depletion

Abstract The locus coeruleus (LC)–norepinephrine (NE) system is an understudied circuit in the context of Alzheimer’s disease (AD), and is thought to play an important role in neurodegenerative and neuropsychiatric diseases involving catecholamine neurotransmitters. Understanding the expression and distribution of the amyloid beta (Aβ) peptide, a primary component of AD, under basal conditions and under conditions of NE perturbation within the coeruleo-cortical pathway may be important for understanding its putative role in pathological states. Thus, the goal of this study is to define expression levels and the subcellular distribution of endogenous Aβ with respect to noradrenergic profiles in the rodent LC and medial prefrontal cortex (mPFC) and, further, to determine the functional relevance of NE in modulating endogenous $ Aβ_{42} $ levels. We report that endogenous $ Aβ_{42} $ is localized to tyrosine hydroxylase (TH) immunoreactive somatodendritic profiles of the LC and dopamine-β-hydroxylase (DβH) immunoreactive axon terminals of the infralimbic mPFC (ILmPFC). Male and female naïve rats have similar levels of amyloid precursor protein (APP) cleavage products demonstrated by western blot, as well as similar levels of endogenous $ Aβ_{42} $ as determined by enzyme-linked immunosorbent assay. Two models of NE depletion, DSP-4 lesion and DβH knockout (KO) mice, were used to assess the functional relevance of NE on endogenous $ Aβ_{42} $ levels. DSP-4 lesioned rats and DβH-KO mice show significantly lower levels of endogenous $ Aβ_{42} $. Noradrenergic depletion did not change APP-cleavage products resulting from β-secretase processing. Thus, resultant decreases in endogenous $ Aβ_{42} $ may be due to decreased neuronal activity of noradrenergic neurons, or, by decreased stimulation of adrenergic receptors which are known to contribute to $ Aβ_{42} $ production by enhancing γ-secretase processing under normal physiological conditions. Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Ross, Jennifer A. [verfasserIn] Reyes, Beverly A. S. [verfasserIn] Thomas, Steven A. [verfasserIn] Van Bockstaele, Elisabeth J. [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2017

Schlagwörter:	Amyloid Norepinephrine Dopamine-β-hydroxylase Adrenergic receptors Stress

Übergeordnetes Werk:	Enthalten in: Anatomy and embryology - Berlin : Springer, 1891, 223(2017), 1 vom: 04. Aug., Seite 267-284
Übergeordnetes Werk:	volume:223 ; year:2017 ; number:1 ; day:04 ; month:08 ; pages:267-284

Links:	Volltext

DOI / URN:	10.1007/s00429-017-1489-9

Katalog-ID:	SPR005731402

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spelling	10.1007/s00429-017-1489-9 doi (DE-627)SPR005731402 (SPR)s00429-017-1489-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.34 bkl Ross, Jennifer A. verfasserin aut Localization of endogenous amyloid-β to the coeruleo-cortical pathway: consequences of noradrenergic depletion 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The locus coeruleus (LC)–norepinephrine (NE) system is an understudied circuit in the context of Alzheimer’s disease (AD), and is thought to play an important role in neurodegenerative and neuropsychiatric diseases involving catecholamine neurotransmitters. Understanding the expression and distribution of the amyloid beta (Aβ) peptide, a primary component of AD, under basal conditions and under conditions of NE perturbation within the coeruleo-cortical pathway may be important for understanding its putative role in pathological states. Thus, the goal of this study is to define expression levels and the subcellular distribution of endogenous Aβ with respect to noradrenergic profiles in the rodent LC and medial prefrontal cortex (mPFC) and, further, to determine the functional relevance of NE in modulating endogenous $ Aβ_{42} $ levels. We report that endogenous $ Aβ_{42} $ is localized to tyrosine hydroxylase (TH) immunoreactive somatodendritic profiles of the LC and dopamine-β-hydroxylase (DβH) immunoreactive axon terminals of the infralimbic mPFC (ILmPFC). Male and female naïve rats have similar levels of amyloid precursor protein (APP) cleavage products demonstrated by western blot, as well as similar levels of endogenous $ Aβ_{42} $ as determined by enzyme-linked immunosorbent assay. Two models of NE depletion, DSP-4 lesion and DβH knockout (KO) mice, were used to assess the functional relevance of NE on endogenous $ Aβ_{42} $ levels. DSP-4 lesioned rats and DβH-KO mice show significantly lower levels of endogenous $ Aβ_{42} $. Noradrenergic depletion did not change APP-cleavage products resulting from β-secretase processing. Thus, resultant decreases in endogenous $ Aβ_{42} $ may be due to decreased neuronal activity of noradrenergic neurons, or, by decreased stimulation of adrenergic receptors which are known to contribute to $ Aβ_{42} $ production by enhancing γ-secretase processing under normal physiological conditions. Amyloid (dpeaa)DE-He213 Norepinephrine (dpeaa)DE-He213 Dopamine-β-hydroxylase (dpeaa)DE-He213 Adrenergic receptors (dpeaa)DE-He213 Stress (dpeaa)DE-He213 Reyes, Beverly A. S. verfasserin aut Thomas, Steven A. verfasserin aut Van Bockstaele, Elisabeth J. verfasserin aut Enthalten in Anatomy and embryology Berlin : Springer, 1891 223(2017), 1 vom: 04. Aug., Seite 267-284 (DE-627)253389798 (DE-600)1458423-2 1432-0568 nnns volume:223 year:2017 number:1 day:04 month:08 pages:267-284 https://dx.doi.org/10.1007/s00429-017-1489-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_711 44.34 ASE AR 223 2017 1 04 08 267-284
allfields_unstemmed	10.1007/s00429-017-1489-9 doi (DE-627)SPR005731402 (SPR)s00429-017-1489-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.34 bkl Ross, Jennifer A. verfasserin aut Localization of endogenous amyloid-β to the coeruleo-cortical pathway: consequences of noradrenergic depletion 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The locus coeruleus (LC)–norepinephrine (NE) system is an understudied circuit in the context of Alzheimer’s disease (AD), and is thought to play an important role in neurodegenerative and neuropsychiatric diseases involving catecholamine neurotransmitters. Understanding the expression and distribution of the amyloid beta (Aβ) peptide, a primary component of AD, under basal conditions and under conditions of NE perturbation within the coeruleo-cortical pathway may be important for understanding its putative role in pathological states. Thus, the goal of this study is to define expression levels and the subcellular distribution of endogenous Aβ with respect to noradrenergic profiles in the rodent LC and medial prefrontal cortex (mPFC) and, further, to determine the functional relevance of NE in modulating endogenous $ Aβ_{42} $ levels. We report that endogenous $ Aβ_{42} $ is localized to tyrosine hydroxylase (TH) immunoreactive somatodendritic profiles of the LC and dopamine-β-hydroxylase (DβH) immunoreactive axon terminals of the infralimbic mPFC (ILmPFC). Male and female naïve rats have similar levels of amyloid precursor protein (APP) cleavage products demonstrated by western blot, as well as similar levels of endogenous $ Aβ_{42} $ as determined by enzyme-linked immunosorbent assay. Two models of NE depletion, DSP-4 lesion and DβH knockout (KO) mice, were used to assess the functional relevance of NE on endogenous $ Aβ_{42} $ levels. DSP-4 lesioned rats and DβH-KO mice show significantly lower levels of endogenous $ Aβ_{42} $. Noradrenergic depletion did not change APP-cleavage products resulting from β-secretase processing. Thus, resultant decreases in endogenous $ Aβ_{42} $ may be due to decreased neuronal activity of noradrenergic neurons, or, by decreased stimulation of adrenergic receptors which are known to contribute to $ Aβ_{42} $ production by enhancing γ-secretase processing under normal physiological conditions. Amyloid (dpeaa)DE-He213 Norepinephrine (dpeaa)DE-He213 Dopamine-β-hydroxylase (dpeaa)DE-He213 Adrenergic receptors (dpeaa)DE-He213 Stress (dpeaa)DE-He213 Reyes, Beverly A. S. verfasserin aut Thomas, Steven A. verfasserin aut Van Bockstaele, Elisabeth J. verfasserin aut Enthalten in Anatomy and embryology Berlin : Springer, 1891 223(2017), 1 vom: 04. Aug., Seite 267-284 (DE-627)253389798 (DE-600)1458423-2 1432-0568 nnns volume:223 year:2017 number:1 day:04 month:08 pages:267-284 https://dx.doi.org/10.1007/s00429-017-1489-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_711 44.34 ASE AR 223 2017 1 04 08 267-284
allfieldsGer	10.1007/s00429-017-1489-9 doi (DE-627)SPR005731402 (SPR)s00429-017-1489-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.34 bkl Ross, Jennifer A. verfasserin aut Localization of endogenous amyloid-β to the coeruleo-cortical pathway: consequences of noradrenergic depletion 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The locus coeruleus (LC)–norepinephrine (NE) system is an understudied circuit in the context of Alzheimer’s disease (AD), and is thought to play an important role in neurodegenerative and neuropsychiatric diseases involving catecholamine neurotransmitters. Understanding the expression and distribution of the amyloid beta (Aβ) peptide, a primary component of AD, under basal conditions and under conditions of NE perturbation within the coeruleo-cortical pathway may be important for understanding its putative role in pathological states. Thus, the goal of this study is to define expression levels and the subcellular distribution of endogenous Aβ with respect to noradrenergic profiles in the rodent LC and medial prefrontal cortex (mPFC) and, further, to determine the functional relevance of NE in modulating endogenous $ Aβ_{42} $ levels. We report that endogenous $ Aβ_{42} $ is localized to tyrosine hydroxylase (TH) immunoreactive somatodendritic profiles of the LC and dopamine-β-hydroxylase (DβH) immunoreactive axon terminals of the infralimbic mPFC (ILmPFC). Male and female naïve rats have similar levels of amyloid precursor protein (APP) cleavage products demonstrated by western blot, as well as similar levels of endogenous $ Aβ_{42} $ as determined by enzyme-linked immunosorbent assay. Two models of NE depletion, DSP-4 lesion and DβH knockout (KO) mice, were used to assess the functional relevance of NE on endogenous $ Aβ_{42} $ levels. DSP-4 lesioned rats and DβH-KO mice show significantly lower levels of endogenous $ Aβ_{42} $. Noradrenergic depletion did not change APP-cleavage products resulting from β-secretase processing. Thus, resultant decreases in endogenous $ Aβ_{42} $ may be due to decreased neuronal activity of noradrenergic neurons, or, by decreased stimulation of adrenergic receptors which are known to contribute to $ Aβ_{42} $ production by enhancing γ-secretase processing under normal physiological conditions. Amyloid (dpeaa)DE-He213 Norepinephrine (dpeaa)DE-He213 Dopamine-β-hydroxylase (dpeaa)DE-He213 Adrenergic receptors (dpeaa)DE-He213 Stress (dpeaa)DE-He213 Reyes, Beverly A. S. verfasserin aut Thomas, Steven A. verfasserin aut Van Bockstaele, Elisabeth J. verfasserin aut Enthalten in Anatomy and embryology Berlin : Springer, 1891 223(2017), 1 vom: 04. Aug., Seite 267-284 (DE-627)253389798 (DE-600)1458423-2 1432-0568 nnns volume:223 year:2017 number:1 day:04 month:08 pages:267-284 https://dx.doi.org/10.1007/s00429-017-1489-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_711 44.34 ASE AR 223 2017 1 04 08 267-284
allfieldsSound	10.1007/s00429-017-1489-9 doi (DE-627)SPR005731402 (SPR)s00429-017-1489-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.34 bkl Ross, Jennifer A. verfasserin aut Localization of endogenous amyloid-β to the coeruleo-cortical pathway: consequences of noradrenergic depletion 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The locus coeruleus (LC)–norepinephrine (NE) system is an understudied circuit in the context of Alzheimer’s disease (AD), and is thought to play an important role in neurodegenerative and neuropsychiatric diseases involving catecholamine neurotransmitters. Understanding the expression and distribution of the amyloid beta (Aβ) peptide, a primary component of AD, under basal conditions and under conditions of NE perturbation within the coeruleo-cortical pathway may be important for understanding its putative role in pathological states. Thus, the goal of this study is to define expression levels and the subcellular distribution of endogenous Aβ with respect to noradrenergic profiles in the rodent LC and medial prefrontal cortex (mPFC) and, further, to determine the functional relevance of NE in modulating endogenous $ Aβ_{42} $ levels. We report that endogenous $ Aβ_{42} $ is localized to tyrosine hydroxylase (TH) immunoreactive somatodendritic profiles of the LC and dopamine-β-hydroxylase (DβH) immunoreactive axon terminals of the infralimbic mPFC (ILmPFC). Male and female naïve rats have similar levels of amyloid precursor protein (APP) cleavage products demonstrated by western blot, as well as similar levels of endogenous $ Aβ_{42} $ as determined by enzyme-linked immunosorbent assay. Two models of NE depletion, DSP-4 lesion and DβH knockout (KO) mice, were used to assess the functional relevance of NE on endogenous $ Aβ_{42} $ levels. DSP-4 lesioned rats and DβH-KO mice show significantly lower levels of endogenous $ Aβ_{42} $. Noradrenergic depletion did not change APP-cleavage products resulting from β-secretase processing. Thus, resultant decreases in endogenous $ Aβ_{42} $ may be due to decreased neuronal activity of noradrenergic neurons, or, by decreased stimulation of adrenergic receptors which are known to contribute to $ Aβ_{42} $ production by enhancing γ-secretase processing under normal physiological conditions. Amyloid (dpeaa)DE-He213 Norepinephrine (dpeaa)DE-He213 Dopamine-β-hydroxylase (dpeaa)DE-He213 Adrenergic receptors (dpeaa)DE-He213 Stress (dpeaa)DE-He213 Reyes, Beverly A. S. verfasserin aut Thomas, Steven A. verfasserin aut Van Bockstaele, Elisabeth J. verfasserin aut Enthalten in Anatomy and embryology Berlin : Springer, 1891 223(2017), 1 vom: 04. Aug., Seite 267-284 (DE-627)253389798 (DE-600)1458423-2 1432-0568 nnns volume:223 year:2017 number:1 day:04 month:08 pages:267-284 https://dx.doi.org/10.1007/s00429-017-1489-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_711 44.34 ASE AR 223 2017 1 04 08 267-284
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source	Enthalten in Anatomy and embryology 223(2017), 1 vom: 04. Aug., Seite 267-284 volume:223 year:2017 number:1 day:04 month:08 pages:267-284
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author	Ross, Jennifer A.
spellingShingle	Ross, Jennifer A. ddc 610 bkl 44.34 misc Amyloid misc Norepinephrine misc Dopamine-β-hydroxylase misc Adrenergic receptors misc Stress Localization of endogenous amyloid-β to the coeruleo-cortical pathway: consequences of noradrenergic depletion
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topic_title	610 ASE 44.34 bkl Localization of endogenous amyloid-β to the coeruleo-cortical pathway: consequences of noradrenergic depletion Amyloid (dpeaa)DE-He213 Norepinephrine (dpeaa)DE-He213 Dopamine-β-hydroxylase (dpeaa)DE-He213 Adrenergic receptors (dpeaa)DE-He213 Stress (dpeaa)DE-He213
topic	ddc 610 bkl 44.34 misc Amyloid misc Norepinephrine misc Dopamine-β-hydroxylase misc Adrenergic receptors misc Stress
topic_unstemmed	ddc 610 bkl 44.34 misc Amyloid misc Norepinephrine misc Dopamine-β-hydroxylase misc Adrenergic receptors misc Stress
topic_browse	ddc 610 bkl 44.34 misc Amyloid misc Norepinephrine misc Dopamine-β-hydroxylase misc Adrenergic receptors misc Stress
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title	Localization of endogenous amyloid-β to the coeruleo-cortical pathway: consequences of noradrenergic depletion
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title_full	Localization of endogenous amyloid-β to the coeruleo-cortical pathway: consequences of noradrenergic depletion
author_sort	Ross, Jennifer A.
journal	Anatomy and embryology
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author_browse	Ross, Jennifer A. Reyes, Beverly A. S. Thomas, Steven A. Van Bockstaele, Elisabeth J.
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title_sort	localization of endogenous amyloid-β to the coeruleo-cortical pathway: consequences of noradrenergic depletion
title_auth	Localization of endogenous amyloid-β to the coeruleo-cortical pathway: consequences of noradrenergic depletion
abstract	Abstract The locus coeruleus (LC)–norepinephrine (NE) system is an understudied circuit in the context of Alzheimer’s disease (AD), and is thought to play an important role in neurodegenerative and neuropsychiatric diseases involving catecholamine neurotransmitters. Understanding the expression and distribution of the amyloid beta (Aβ) peptide, a primary component of AD, under basal conditions and under conditions of NE perturbation within the coeruleo-cortical pathway may be important for understanding its putative role in pathological states. Thus, the goal of this study is to define expression levels and the subcellular distribution of endogenous Aβ with respect to noradrenergic profiles in the rodent LC and medial prefrontal cortex (mPFC) and, further, to determine the functional relevance of NE in modulating endogenous $ Aβ_{42} $ levels. We report that endogenous $ Aβ_{42} $ is localized to tyrosine hydroxylase (TH) immunoreactive somatodendritic profiles of the LC and dopamine-β-hydroxylase (DβH) immunoreactive axon terminals of the infralimbic mPFC (ILmPFC). Male and female naïve rats have similar levels of amyloid precursor protein (APP) cleavage products demonstrated by western blot, as well as similar levels of endogenous $ Aβ_{42} $ as determined by enzyme-linked immunosorbent assay. Two models of NE depletion, DSP-4 lesion and DβH knockout (KO) mice, were used to assess the functional relevance of NE on endogenous $ Aβ_{42} $ levels. DSP-4 lesioned rats and DβH-KO mice show significantly lower levels of endogenous $ Aβ_{42} $. Noradrenergic depletion did not change APP-cleavage products resulting from β-secretase processing. Thus, resultant decreases in endogenous $ Aβ_{42} $ may be due to decreased neuronal activity of noradrenergic neurons, or, by decreased stimulation of adrenergic receptors which are known to contribute to $ Aβ_{42} $ production by enhancing γ-secretase processing under normal physiological conditions.
abstractGer	Abstract The locus coeruleus (LC)–norepinephrine (NE) system is an understudied circuit in the context of Alzheimer’s disease (AD), and is thought to play an important role in neurodegenerative and neuropsychiatric diseases involving catecholamine neurotransmitters. Understanding the expression and distribution of the amyloid beta (Aβ) peptide, a primary component of AD, under basal conditions and under conditions of NE perturbation within the coeruleo-cortical pathway may be important for understanding its putative role in pathological states. Thus, the goal of this study is to define expression levels and the subcellular distribution of endogenous Aβ with respect to noradrenergic profiles in the rodent LC and medial prefrontal cortex (mPFC) and, further, to determine the functional relevance of NE in modulating endogenous $ Aβ_{42} $ levels. We report that endogenous $ Aβ_{42} $ is localized to tyrosine hydroxylase (TH) immunoreactive somatodendritic profiles of the LC and dopamine-β-hydroxylase (DβH) immunoreactive axon terminals of the infralimbic mPFC (ILmPFC). Male and female naïve rats have similar levels of amyloid precursor protein (APP) cleavage products demonstrated by western blot, as well as similar levels of endogenous $ Aβ_{42} $ as determined by enzyme-linked immunosorbent assay. Two models of NE depletion, DSP-4 lesion and DβH knockout (KO) mice, were used to assess the functional relevance of NE on endogenous $ Aβ_{42} $ levels. DSP-4 lesioned rats and DβH-KO mice show significantly lower levels of endogenous $ Aβ_{42} $. Noradrenergic depletion did not change APP-cleavage products resulting from β-secretase processing. Thus, resultant decreases in endogenous $ Aβ_{42} $ may be due to decreased neuronal activity of noradrenergic neurons, or, by decreased stimulation of adrenergic receptors which are known to contribute to $ Aβ_{42} $ production by enhancing γ-secretase processing under normal physiological conditions.
abstract_unstemmed	Abstract The locus coeruleus (LC)–norepinephrine (NE) system is an understudied circuit in the context of Alzheimer’s disease (AD), and is thought to play an important role in neurodegenerative and neuropsychiatric diseases involving catecholamine neurotransmitters. Understanding the expression and distribution of the amyloid beta (Aβ) peptide, a primary component of AD, under basal conditions and under conditions of NE perturbation within the coeruleo-cortical pathway may be important for understanding its putative role in pathological states. Thus, the goal of this study is to define expression levels and the subcellular distribution of endogenous Aβ with respect to noradrenergic profiles in the rodent LC and medial prefrontal cortex (mPFC) and, further, to determine the functional relevance of NE in modulating endogenous $ Aβ_{42} $ levels. We report that endogenous $ Aβ_{42} $ is localized to tyrosine hydroxylase (TH) immunoreactive somatodendritic profiles of the LC and dopamine-β-hydroxylase (DβH) immunoreactive axon terminals of the infralimbic mPFC (ILmPFC). Male and female naïve rats have similar levels of amyloid precursor protein (APP) cleavage products demonstrated by western blot, as well as similar levels of endogenous $ Aβ_{42} $ as determined by enzyme-linked immunosorbent assay. Two models of NE depletion, DSP-4 lesion and DβH knockout (KO) mice, were used to assess the functional relevance of NE on endogenous $ Aβ_{42} $ levels. DSP-4 lesioned rats and DβH-KO mice show significantly lower levels of endogenous $ Aβ_{42} $. Noradrenergic depletion did not change APP-cleavage products resulting from β-secretase processing. Thus, resultant decreases in endogenous $ Aβ_{42} $ may be due to decreased neuronal activity of noradrenergic neurons, or, by decreased stimulation of adrenergic receptors which are known to contribute to $ Aβ_{42} $ production by enhancing γ-secretase processing under normal physiological conditions.
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title_short	Localization of endogenous amyloid-β to the coeruleo-cortical pathway: consequences of noradrenergic depletion
url	https://dx.doi.org/10.1007/s00429-017-1489-9
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author2	Reyes, Beverly A. S. Thomas, Steven A. Van Bockstaele, Elisabeth J.
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up_date	2024-07-03T18:18:56.742Z
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Localization of endogenous amyloid-β to the coeruleo-cortical pathway: consequences of noradrenergic depletion

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