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Hydroxyurea protects hippocampal neurons against oxidative, metabolic and excitotoxic stress, and improves spatial memory in a mouse model of Alzheimer’s disease (Rat)

ABSTRACT: Hydroxyurea protects hippocampal neurons against oxidative, metabolic and excitotoxic stress, and improves spatial memory in a mouse model of Alzheimer’s disease (Rat)

PROVIDER: PRJNA438665 | ENA |

REPOSITORIES: ENA

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Hydroxyurea protects hippocampal neurons against oxidative, metabolic and excitotoxic stress, and improves spatial memory in a mouse model of Alzheimer’s disease (Rat)

Project description:Alzheimer’s disease (AD) is an age-related neurodegenerative disorder characterized by accumulation of amyloid β-peptide (Aβ) plaques in the brain and decreased cognitive function leading to dementia. We determined if hydroxyurea (HU), a ribonucleotide reductase inhibitor known to activate adaptive cellular stress responses in fibroblasts, could protect rat hippocampal neurons against oxidative-, excitatory-, mitochondrial-, and Aβ-induced stress and if HU treatment could improve learning and memory in a mouse model of AD (APP/PS1 double mutant transgenic mice). HU treatment attenuated the loss of cell viability induced by treatment of hippocampal neurons with hydrogen peroxide, glutamate, rotenone, and Aβ1-42. HU treatment also attenuated reductions of mitochondrial reserve capacity, maximal respiration, and cellular ATP content induced by hydrogen peroxide treatment. In vivo, treatment of APP/PS1 AD mice with HU (45 mg/kg/day) improved spatial memory performance in the hippocampus-dependent Morris water maze task. In summary, HU provides neuroprotection against toxic insults, improves mitochondrial bioenergetics, and improves spatial memory in a mouse model of AD. HU may offer a new therapeutic approach to delay cognitive decline in AD.

2018-09-10 | GSE111941 | GEO

Hydroxyurea protects hippocampal neurons against oxidative, metabolic and excitotoxic stress, and improves spatial memory in a mouse model of Alzheimer’s disease (Mouse)

2018-09-10 | GSE111940 | GEO

Hydroxyurea protects hippocampal neurons against oxidative, metabolic and excitotoxic stress, and improves spatial memory in a mouse model of Alzheimer’s disease (Mouse)

Project description:Hydroxyurea protects hippocampal neurons against oxidative, metabolic and excitotoxic stress, and improves spatial memory in a mouse model of Alzheimer’s disease (Mouse)

| PRJNA438664 | ENA

Hydroxyurea attenuates oxidative, metabolic, and excitotoxic stress in rat hippocampal neurons and improves spatial memory in a mouse model of Alzheimer’s disease

Project description:Hydroxyurea attenuates oxidative, metabolic, and excitotoxic stress in rat hippocampal neurons and improves spatial memory in a mouse model of Alzheimer’s disease

| PRJNA438652 | ENA

Oxidative Stress Mechanisms of Hydroxyurea-Induced Developmetal Toxicity in Organogenesis Stage Mouse Embryos

Project description:To investigate the gene expression changes in gestational day 9 embryos exposed to hydroxyurea in utero. Agilent microarray technology was used to identify genes that responded to hydroxyurea exposure. Understanding the stress response of the embryo will help us advance education of birth defect prevention. Gestational day 9 embryos were exposed to 400 mg/kg hydroxyurea, a dose that induces a moderate number of malformations, including fetal resorptions, growth retardation, external and skeletal defects. We identified several genes involved in responding to oxidative stress, including NRF-2, PRDX1, and TXNIP. Other genes also significantly changed were involved in cell cycle arrest and apoptosis. The dysregulation in gene expression during organogenesis contributes to the developmental toxicity of hydroxyurea. Gestational day 9 mouse embryos were treated with saline or 400 mg/kg hydroxyurea by intraperitoneal injection. Dams were euthanized after 3 hours and embryos explanted. 6 indendent experiments were performed for each sample.

2015-01-15 | E-GEOD-54579 | biostudies-arrayexpress

Hydroxyurea attenuates oxidative, metabolic, and excitotoxic stress in rat hippocampal neurons and improves spatial memory in a mouse model of Alzheimer’s disease

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-09-10 | GSE111943 | GEO

Gas6 improves plaque burden, yet worsens behavior and induces microglial inflammation in the APP/PS1 model of Alzheimer’s disease

Project description:We sought to determine the effects of Gas6 on Alzheimer’s disease pathology through overexpression of Gas6 using an adeno-associated viral vector in the APP/PS1 model of Alzheimer’s disease. 9 month old male and female APP/PS1 and nontransgenic littermates received bilateral stereotactic hippocampal injections of AAV-Gas6 or AAV-control, an attenuated Gas6 protein that does not bind the Axl receptor. One month after injections, mice performed a battery of behavioral tasks and brains were processed for immunohistochemistry, transcriptional analyses, and flow cytometry.

2022-03-30 | GSE171195 | GEO

Sleep-active hypothalamic MCH-system modulates hippocampal synaptic plasticity and is vulnerable in early Alzheimer’s Disease

Project description:In Alzheimer’s disease (AD), pathophysiological changes in the hippocampus cause deficits in episodic memory formation, leading to cognitive impairment. Hippocampal hyperactivity and decreased sleep quality are associated with early AD, but their basis is poorly understood. We find that homeostatic mechanisms transiently counteract increased excitatory drive of hippocampal CA1 neurons in AppNL-G-F mice, but fail to stabilize it at control levels. Spatial transcriptomics (ST) analysis identifies the Pmch gene encoding Melanin-Concentrating Hormone (MCH) as part of the adaptive response in AppNL-G-F mice. Hypothalamic MCH peptide is produced in sleep-active lateral hypothalamic neurons that project to CA1 and modulate memory. We show that MCH downregulates synaptic transmission and modulates firing rate homeostasis in hippocampal neurons. Moreover, MCH reverses the increased excitatory drive of CA1 neurons in AppNL-G-F mice. Consistent with our finding that a reduced fraction of MCH-neurons is active in AppNL-G-F mice, these animals spend less time in rapid eye movement (REM) sleep. In addition, MCH-axons projecting to CA1 become progressively impaired in both AppNL-G-F mice and AD patients. Our findings identify the MCH-system as vulnerable in early AD and suggest that impaired MCH-system function contributes to aberrant excitatory drive and sleep defects, which can compromise hippocampal-dependent functions.

2023-09-07 | GSE225181 | GEO

Single-nucleus RNA sequencing reveals transcriptional changes of hippocampal neurons in APP23 mouse model of Alzheimer’s disease

Project description:Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that mostly strikes the elderly. However, the exact molecular and cellular pathogenesis of AD, especially the dynamic changes of neurons during disease progression, remains poorly understood. Here we used single-nucleus RNA sequencing (snRNA-seq) to access the transcriptional changes of hippocampal neurons in APP23 mouse model of AD. We performed snRNA-seq using a modified Smart-seq2 technique on 3,280 neuronal nuclei from the hippocampus of young and aged APP23 and control mice and identified four distinct subpopulations. Comparative transcriptional analysis showed multiple changes in different subtypes of hippocampal neurons of APP23 mice in comparison to control mice, as well as the transcriptional changes in these neurons during disease progression. Our findings revealed multiple neuronal subtype-specific transcriptional changes that may lead to targets for future studies of AD.

2019-11-27 | GSE141044 | GEO

Tn-seq of hydroxyurea treated Bacillus subtilis cells

Project description:Hydroxyurea (HU) is thought to primarily target ribonucleotide reductase (RNR), therefore inhibiting the conversion of rNTPs into dNTPs and slowing DNA replication. To understand how Bacillus subtilis responds to HU stress, we performed RNA-seq and Tn-seq. We obtained genes with fitness defects following hydroxyurea treatment over 3 growth periods.

2021-03-29 | GSE169564 | GEO

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