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Treatment of beta amyloid 1–42 (Aβ1–42)-induced basal forebrain cholinergic damage by a non-classical estrogen signaling activator in vivo
by
Kwakowsky, Andrea
, Peppercorn, Katie
, Potapov, Kyoko
, Ábrahám, István M.
, Kim, SooHyun
, Tate, Warren P.
in
13
/ 13/51
/ 14
/ 14/1
/ 14/19
/ 17β-Estradiol
/ 631/378
/ 631/378/1689/1283
/ 64
/ 64/60
/ 692/163
/ 96
/ 96/95
/ Alzheimer's disease
/ Amyloid beta-Peptides - metabolism
/ Amyloid beta-Peptides - pharmacology
/ Animals
/ Basal forebrain
/ Basal Forebrain - drug effects
/ Basal Forebrain - metabolism
/ Basal Forebrain - pathology
/ Cell Count
/ Cholinergic Fibers - drug effects
/ Cholinergic Fibers - metabolism
/ Cholinergic Fibers - pathology
/ Cholinergic Neurons - drug effects
/ Cholinergic Neurons - metabolism
/ Cholinergic Neurons - pathology
/ Cognitive ability
/ Cortex
/ Estrogen Receptor alpha - metabolism
/ Estrogens
/ Estrogens - metabolism
/ Estrogens - pharmacology
/ Female
/ Fibers
/ Forebrain
/ Humanities and Social Sciences
/ Injection
/ Innervation
/ Intracellular
/ Intracellular signalling
/ Learning - drug effects
/ Mice
/ Mice, Knockout
/ multidisciplinary
/ Neurodegenerative diseases
/ Neurons
/ Neuroprotection
/ Peptide Fragments - metabolism
/ Peptide Fragments - pharmacology
/ Phosphorylation
/ Rodents
/ Science
/ Side effects
/ Signal transduction
/ Signal Transduction - drug effects
/ Somatosensory Cortex - drug effects
/ Somatosensory Cortex - metabolism
/ Somatosensory Cortex - pathology
/ Xenoestrogens
/ β-Amyloid
2016
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Treatment of beta amyloid 1–42 (Aβ1–42)-induced basal forebrain cholinergic damage by a non-classical estrogen signaling activator in vivo
by
Kwakowsky, Andrea
, Peppercorn, Katie
, Potapov, Kyoko
, Ábrahám, István M.
, Kim, SooHyun
, Tate, Warren P.
in
13
/ 13/51
/ 14
/ 14/1
/ 14/19
/ 17β-Estradiol
/ 631/378
/ 631/378/1689/1283
/ 64
/ 64/60
/ 692/163
/ 96
/ 96/95
/ Alzheimer's disease
/ Amyloid beta-Peptides - metabolism
/ Amyloid beta-Peptides - pharmacology
/ Animals
/ Basal forebrain
/ Basal Forebrain - drug effects
/ Basal Forebrain - metabolism
/ Basal Forebrain - pathology
/ Cell Count
/ Cholinergic Fibers - drug effects
/ Cholinergic Fibers - metabolism
/ Cholinergic Fibers - pathology
/ Cholinergic Neurons - drug effects
/ Cholinergic Neurons - metabolism
/ Cholinergic Neurons - pathology
/ Cognitive ability
/ Cortex
/ Estrogen Receptor alpha - metabolism
/ Estrogens
/ Estrogens - metabolism
/ Estrogens - pharmacology
/ Female
/ Fibers
/ Forebrain
/ Humanities and Social Sciences
/ Injection
/ Innervation
/ Intracellular
/ Intracellular signalling
/ Learning - drug effects
/ Mice
/ Mice, Knockout
/ multidisciplinary
/ Neurodegenerative diseases
/ Neurons
/ Neuroprotection
/ Peptide Fragments - metabolism
/ Peptide Fragments - pharmacology
/ Phosphorylation
/ Rodents
/ Science
/ Side effects
/ Signal transduction
/ Signal Transduction - drug effects
/ Somatosensory Cortex - drug effects
/ Somatosensory Cortex - metabolism
/ Somatosensory Cortex - pathology
/ Xenoestrogens
/ β-Amyloid
2016
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While trying to remove the title from your shelf something went wrong :( Kindly try again later!
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Treatment of beta amyloid 1–42 (Aβ1–42)-induced basal forebrain cholinergic damage by a non-classical estrogen signaling activator in vivo
by
Kwakowsky, Andrea
, Peppercorn, Katie
, Potapov, Kyoko
, Ábrahám, István M.
, Kim, SooHyun
, Tate, Warren P.
in
13
/ 13/51
/ 14
/ 14/1
/ 14/19
/ 17β-Estradiol
/ 631/378
/ 631/378/1689/1283
/ 64
/ 64/60
/ 692/163
/ 96
/ 96/95
/ Alzheimer's disease
/ Amyloid beta-Peptides - metabolism
/ Amyloid beta-Peptides - pharmacology
/ Animals
/ Basal forebrain
/ Basal Forebrain - drug effects
/ Basal Forebrain - metabolism
/ Basal Forebrain - pathology
/ Cell Count
/ Cholinergic Fibers - drug effects
/ Cholinergic Fibers - metabolism
/ Cholinergic Fibers - pathology
/ Cholinergic Neurons - drug effects
/ Cholinergic Neurons - metabolism
/ Cholinergic Neurons - pathology
/ Cognitive ability
/ Cortex
/ Estrogen Receptor alpha - metabolism
/ Estrogens
/ Estrogens - metabolism
/ Estrogens - pharmacology
/ Female
/ Fibers
/ Forebrain
/ Humanities and Social Sciences
/ Injection
/ Innervation
/ Intracellular
/ Intracellular signalling
/ Learning - drug effects
/ Mice
/ Mice, Knockout
/ multidisciplinary
/ Neurodegenerative diseases
/ Neurons
/ Neuroprotection
/ Peptide Fragments - metabolism
/ Peptide Fragments - pharmacology
/ Phosphorylation
/ Rodents
/ Science
/ Side effects
/ Signal transduction
/ Signal Transduction - drug effects
/ Somatosensory Cortex - drug effects
/ Somatosensory Cortex - metabolism
/ Somatosensory Cortex - pathology
/ Xenoestrogens
/ β-Amyloid
2016
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Treatment of beta amyloid 1–42 (Aβ1–42)-induced basal forebrain cholinergic damage by a non-classical estrogen signaling activator in vivo
Journal Article
Treatment of beta amyloid 1–42 (Aβ1–42)-induced basal forebrain cholinergic damage by a non-classical estrogen signaling activator in vivo
2016
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Overview
In Alzheimer’s disease (AD), there is a loss in cholinergic innervation targets of basal forebrain which has been implicated in substantial cognitive decline. Amyloid beta peptide (Aβ
1–42
) accumulates in AD that is highly toxic for basal forebrain cholinergic (BFC) neurons. Although the gonadal steroid estradiol is neuroprotective, the administration is associated with risk of off-target effects. Previous findings suggested that non-classical estradiol action on intracellular signaling pathways has ameliorative potential without estrogenic side effects. After Aβ
1–42
injection into mouse basal forebrain, a single dose of 4-estren-3α, 17β-diol (estren), the non-classical estradiol pathway activator, restored loss of cholinergic cortical projections and also attenuated the Aβ
1–42
-induced learning deficits. Estren rapidly and directly phosphorylates c-AMP-response–element-binding-protein and extracellular-signal-regulated-kinase-1/2 in BFC neurons and restores the cholinergic fibers via estrogen receptor-α. These findings indicated that selective activation of non-classical intracellular estrogen signaling has a potential to treat the damage of cholinergic neurons in AD.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 13/51
/ 14
/ 14/1
/ 14/19
/ 631/378
/ 64
/ 64/60
/ 692/163
/ 96
/ 96/95
/ Amyloid beta-Peptides - metabolism
/ Amyloid beta-Peptides - pharmacology
/ Animals
/ Basal Forebrain - drug effects
/ Basal Forebrain - metabolism
/ Cholinergic Fibers - drug effects
/ Cholinergic Fibers - metabolism
/ Cholinergic Fibers - pathology
/ Cholinergic Neurons - drug effects
/ Cholinergic Neurons - metabolism
/ Cholinergic Neurons - pathology
/ Cortex
/ Estrogen Receptor alpha - metabolism
/ Female
/ Fibers
/ Humanities and Social Sciences
/ Mice
/ Neurons
/ Peptide Fragments - metabolism
/ Peptide Fragments - pharmacology
/ Rodents
/ Science
/ Signal Transduction - drug effects
/ Somatosensory Cortex - drug effects
/ Somatosensory Cortex - metabolism
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