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Article ; Online: Early Life Obesity Increases Neuroinflammation, Amyloid Beta Deposition, and Cognitive Decline in a Mouse Model of Alzheimer's Disease.

So, Simon W / Fleming, Kendra M / Nixon, Joshua P / Butterick, Tammy A

2023 Volume 15, Issue 11

Abstract: Obesity, a known risk factor of Alzheimer's disease (AD), increases the activation of microglia, leading to a proinflammatory phenotype. Our previous work shows that a high fat diet (HFD) can cause neuroinflammation and cognitive decline in mice. We ... ...

Abstract	Obesity, a known risk factor of Alzheimer's disease (AD), increases the activation of microglia, leading to a proinflammatory phenotype. Our previous work shows that a high fat diet (HFD) can cause neuroinflammation and cognitive decline in mice. We hypothesized that proinflammatory activation of brain microglia in obesity exacerbates AD pathology and increases the accumulation of amyloid beta (Aβ) plaques. Presently, we tested cognitive function in 8-month-old male and female APP/PS1 mice fed a HFD, starting at 1.5 months of age. Locomotor activity, anxiety-like behavior, behavioral despair, and spatial memory were all assessed through behavioral tests. Microgliosis and Aβ deposition were measured in multiple brain regions through immunohistochemical analysis. Our results show that a HFD decreases locomotor activity, while increasing anxiety-like behavior and behavioral despair independent of genotype. A HFD led to increased memory deficits in both sexes, with HFD-fed APP/PS1 mice performing the worst out of all groups. Immunohistochemical analysis showed increased microgliosis in mice fed a HFD. This was accompanied by an increase in Aβ deposition in the HFD-fed APP/PS1 mice. Together, our results support that HFD-induced obesity exacerbates neuroinflammation and Aβ deposition in a young adult AD mouse model, leading to increased memory deficits and cognitive decline in both sexes.
MeSH term(s)	Male ; Mice ; Female ; Animals ; Alzheimer Disease/genetics ; Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Neuroinflammatory Diseases ; Mice, Transgenic ; Memory Disorders/complications ; Cognitive Dysfunction/complications ; Disease Models, Animal ; Plaque, Amyloid/genetics ; Obesity/complications ; Presenilin-1/genetics
Chemical Substances	Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Presenilin-1
Language	English
Publishing date	2023-05-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu15112494
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: RNAseq Analysis of FABP4 Knockout Mouse Hippocampal Transcriptome Suggests a Role for WNT/β-Catenin in Preventing Obesity-Induced Cognitive Impairment.

So, Simon W / Nixon, Joshua P / Bernlohr, David A / Butterick, Tammy A

International journal of molecular sciences

2023 Volume 24, Issue 4

Abstract: Microglial fatty-acid binding protein 4 (FABP4) is a regulator of neuroinflammation. We hypothesized that the link between lipid metabolism and inflammation indicates a role for FABP4 in regulating high fat diet (HFD)-induced cognitive decline. We have ... ...

Abstract	Microglial fatty-acid binding protein 4 (FABP4) is a regulator of neuroinflammation. We hypothesized that the link between lipid metabolism and inflammation indicates a role for FABP4 in regulating high fat diet (HFD)-induced cognitive decline. We have previously shown that obese FABP4 knockout mice exhibit decreased neuroinflammation and cognitive decline. FABP4 knockout and wild type mice were fed 60% HFD for 12 weeks starting at 15 weeks old. Hippocampal tissue was dissected and RNA-seq was performed to measure differentially expressed transcripts. Reactome molecular pathway analysis was utilized to examine differentially expressed pathways. Results showed that HFD-fed FABP4 knockout mice have a hippocampal transcriptome consistent with neuroprotection, including associations with decreased proinflammatory signaling, ER stress, apoptosis, and cognitive decline. This is accompanied by an increase in transcripts upregulating neurogenesis, synaptic plasticity, long-term potentiation, and spatial working memory. Pathway analysis revealed that mice lacking FABP4 had changes in metabolic function that support reduction in oxidative stress and inflammation, and improved energy homeostasis and cognitive function. Analysis suggested a role for WNT/β-Catenin signaling in the protection against insulin resistance, alleviating neuroinflammation and cognitive decline. Collectively, our work shows that FABP4 represents a potential target in alleviating HFD-induced neuroinflammation and cognitive decline and suggests a role for WNT/β-Catenin in this protection.
MeSH term(s)	Animals ; Mice ; beta Catenin/metabolism ; Cognitive Dysfunction/metabolism ; Diet, High-Fat ; Fatty Acid-Binding Proteins/metabolism ; Hippocampus/metabolism ; Inflammation/metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; Neuroinflammatory Diseases ; Obesity/metabolism ; Transcriptome ; Wnt Signaling Pathway
Chemical Substances	beta Catenin ; Fabp4 protein, mouse ; Fatty Acid-Binding Proteins ; CTNNB1 protein, mouse
Language	English
Publishing date	2023-02-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24043381
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Article ; Online: Microglial FABP4-UCP2 Axis Modulates Neuroinflammation and Cognitive Decline in Obese Mice.

So, Simon W / Fleming, Kendra M / Duffy, Cayla M / Nixon, Joshua P / Bernlohr, David A / Butterick, Tammy A

International journal of molecular sciences

2022 Volume 23, Issue 8

Abstract: The microglial fatty-acid-binding protein 4-uncoupling protein 2 (FABP4-UCP2) axis is a key regulator of neuroinflammation in high-fat-diet (HFD)-fed animals, indicating a role for FABP4 in brain immune response. We hypothesized that the FABP4-UCP2 axis ... ...

Abstract	The microglial fatty-acid-binding protein 4-uncoupling protein 2 (FABP4-UCP2) axis is a key regulator of neuroinflammation in high-fat-diet (HFD)-fed animals, indicating a role for FABP4 in brain immune response. We hypothesized that the FABP4-UCP2 axis is involved in regulating diet-induced cognitive decline. We tested cognitive function in mice lacking microglial FABP4 (AKO mice). Fifteen-week-old male AKO and wild-type (WT) mice were maintained on 60% HFD or normal chow (NC) for 12 weeks. Body composition was measured using EchoMRI. Locomotor activity, working memory, and spatial memory were assessed using behavioral tests (open field, T-maze, and Barnes maze, respectively). Hippocampal microgliosis was assessed via immunohistochemical staining. An inflammatory cytokine panel was assayed using hippocampal tissue. Real-time RT-PCR was performed to measure microglial UCP2 mRNA expression. Our data support that loss of FABP4 prevents cognitive decline in vivo. HFD-fed WT mice exhibited impaired long- and short-term memory, in contrast with HFD-fed AKO mice. HFD-fed WT mice had an increase in hippocampal inflammatory cytokine expression (IFNγ, IL-1β, IL-5, IL-6, KC/GRO(CXCL1), IL-10, and TNFα) and microgliosis, and decreased microglial UCP2 expression. HFD-fed AKO mice had decreased hippocampal inflammatory cytokine expression and microgliosis and increased microglial UCP2 expression compared to HFD-fed WT mice. Collectively, our work supports the idea that the FABP4-UCP2 axis represents a potential therapeutic target in preventing diet-induced cognitive decline.
MeSH term(s)	Animals ; Cognitive Dysfunction/etiology ; Cognitive Dysfunction/metabolism ; Diet, High-Fat/adverse effects ; Fatty Acid-Binding Proteins/genetics ; Fatty Acid-Binding Proteins/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Microglia/metabolism ; Neuroinflammatory Diseases ; Uncoupling Protein 2/genetics ; Uncoupling Protein 2/metabolism
Chemical Substances	Fabp4 protein, mouse ; Fatty Acid-Binding Proteins ; Ucp2 protein, mouse ; Uncoupling Protein 2
Language	English
Publishing date	2022-04-14
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23084354
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Article ; Online: Microglial FABP4-UCP2 Axis Modulates Neuroinflammation and Cognitive Decline in Obese Mice

Simon W. So / Kendra M. Fleming / Cayla M. Duffy / Joshua P. Nixon / David A. Bernlohr / Tammy A. Butterick

International Journal of Molecular Sciences, Vol 23, Iss 4354, p

2022 Volume 4354

Abstract	The microglial fatty-acid-binding protein 4-uncoupling protein 2 (FABP4-UCP2) axis is a key regulator of neuroinflammation in high-fat-diet (HFD)-fed animals, indicating a role for FABP4 in brain immune response. We hypothesized that the FABP4-UCP2 axis is involved in regulating diet-induced cognitive decline. We tested cognitive function in mice lacking microglial FABP4 (AKO mice). Fifteen-week-old male AKO and wild-type (WT) mice were maintained on 60% HFD or normal chow (NC) for 12 weeks. Body composition was measured using EchoMRI. Locomotor activity, working memory, and spatial memory were assessed using behavioral tests (open field, T-maze, and Barnes maze, respectively). Hippocampal microgliosis was assessed via immunohistochemical staining. An inflammatory cytokine panel was assayed using hippocampal tissue. Real-time RT-PCR was performed to measure microglial UCP2 mRNA expression. Our data support that loss of FABP4 prevents cognitive decline in vivo. HFD-fed WT mice exhibited impaired long- and short-term memory, in contrast with HFD-fed AKO mice. HFD-fed WT mice had an increase in hippocampal inflammatory cytokine expression (IFNγ, IL-1β, IL-5, IL-6, KC/GRO(CXCL1), IL-10, and TNFα) and microgliosis, and decreased microglial UCP2 expression. HFD-fed AKO mice had decreased hippocampal inflammatory cytokine expression and microgliosis and increased microglial UCP2 expression compared to HFD-fed WT mice. Collectively, our work supports the idea that the FABP4-UCP2 axis represents a potential therapeutic target in preventing diet-induced cognitive decline.
Keywords	FABP4 ; UCP2 ; microglia ; cognitive decline ; neuroinflammation ; obesity ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	616
Language	English
Publishing date	2022-04-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Whole-body inhalation of nano-sized carbon black: a surrogate model of military burn pit exposure.

Trembley, Janeen H / So, Simon W / Nixon, Joshua P / Bowdridge, Elizabeth C / Garner, Krista L / Griffith, Julie / Engles, Kevin J / Batchelor, Thomas P / Goldsmith, William T / Tomáška, Julie M / Hussain, Salik / Nurkiewicz, Timothy R / Butterick, Tammy A

BMC research notes

2022 Volume 15, Issue 1, Page(s) 275

Abstract: Objective: Chronic multisymptom illness (CMI) is an idiopathic disease affecting thousands of U.S. Veterans exposed to open-air burn pits emitting aerosolized particulate matter (PM) while serving in Central and Southwest Asia and Africa. Exposure to ... ...

Abstract	Objective: Chronic multisymptom illness (CMI) is an idiopathic disease affecting thousands of U.S. Veterans exposed to open-air burn pits emitting aerosolized particulate matter (PM) while serving in Central and Southwest Asia and Africa. Exposure to burn pit PM can result in profound biologic consequences including chronic fatigue, impaired cognition, and respiratory diseases. Dysregulated or unresolved inflammation is a possible underlying mechanism for CMI onset. We describe a rat model of whole-body inhalation exposure using carbon black nanoparticles (CB) as a surrogate for military burn pit-related exposure. Using this model, we measured biomarkers of inflammation in multiple tissues. Results: Male Sprague Dawley rats were exposed to CB aerosols by whole body inhalation (6 ± 0.83 mg/m
MeSH term(s)	Animals ; Biomarkers ; Carbon ; Chronic Disease ; Incineration ; Inflammation ; Inhalation Exposure/adverse effects ; Lung ; Male ; Rats ; Rats, Sprague-Dawley ; Soot/toxicity
Chemical Substances	Biomarkers ; Soot ; Carbon (7440-44-0)
Language	English
Publishing date	2022-08-11
Publishing country	England
Document type	Journal Article
ZDB-ID	2413336-X
ISSN	1756-0500 ; 1756-0500
ISSN (online)	1756-0500
ISSN	1756-0500
DOI	10.1186/s13104-022-06165-2
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Article ; Online: Persistent diastolic dysfunction in chronically ischemic hearts following coronary artery bypass graft.

Aggarwal, Rishav / Qi, Steven S / So, Simon W / Swingen, Cory / Reyes, Christina P / Rose, Rebecca / Wright, Christin / Hocum Stone, Laura L / Nixon, Joshua P / McFalls, Edward O / Butterick, Tammy A / Kelly, Rosemary F

The Journal of thoracic and cardiovascular surgery

2022 Volume 165, Issue 6, Page(s) e269–e279

Abstract: ... Diastolic peak filling rate was lower in HIB compared with control (5.4 ± 0.7 vs 6.7 ± 1.4 respectively, P ... 002), with near recovery with CABG (6.3 ± 0.8, P = .06). Cardiac MRI confirmed preserved global ...

Abstract	Objective: A porcine model was used to study diastolic dysfunction in hibernating myocardium (HM) and recovery with coronary artery bypass surgery (CABG). Methods: HM was induced in Yorkshire-Landrace juvenile swine (n = 30) by placing a c-constrictor on left anterior descending artery causing chronic myocardial ischemia without infarction. At 12 weeks, animals developed the HM phenotype and were either killed humanely (HIB group; n = 11) or revascularized with CABG and allowed 4 weeks of recovery (HIB+CABG group; n = 19). Control pigs were matched for weight, age, and sex to the HIB group. Before the animals were killed humanely, cardiac magnetic resonance imaging (MRI) was done at rest and during a low-dose dobutamine infusion. Tissue was obtained for histologic and proinflammatory biomarker analyses. Results: Diastolic peak filling rate was lower in HIB compared with control (5.4 ± 0.7 vs 6.7 ± 1.4 respectively, P = .002), with near recovery with CABG (6.3 ± 0.8, P = .06). Cardiac MRI confirmed preserved global systolic function in all groups. Histology confirmed there was no transmural infarction but showed interstitial fibrosis in the endomysium in both the HIB and HIB+CABG groups compared with normal myocardium. Alpha-smooth muscle actin stain identified increased myofibroblasts in HM that were less apparent post-CABG. Cytokine and proteomic studies in HM showed decreased peroxisome proliferator-activator receptor gamma coactivator 1-alpha (PGC1-α) expression but increased expression of granulocyte-macrophage colony-stimulating factor and nuclear factor kappa-light-chain enhancer of activated B cells (NFκB). Following CABG, PGC1-α and NFκB expression returned to control whereas granulocyte-macrophage colony-stimulating factor, tumor necrosis factor-α, and interferon gamma remained increased. Conclusions: In porcine model of HM, increased NFκB expression, enhanced myofibroblasts, and collagen deposition along with decreased PGC1-α expression were observed, all of which tended toward normal with CABG. Estimates of impaired relaxation with MRI within HM during increased workload persisted despite CABG, suggesting a need for adjuvant therapies during revascularization.
MeSH term(s)	Swine ; Animals ; Granulocyte-Macrophage Colony-Stimulating Factor/therapeutic use ; Proteomics ; Myocardial Stunning ; Coronary Artery Bypass/adverse effects ; Coronary Artery Bypass/methods ; Infarction
Chemical Substances	Granulocyte-Macrophage Colony-Stimulating Factor (83869-56-1)
Language	English
Publishing date	2022-08-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3104-5
ISSN	1097-685X ; 0022-5223
ISSN (online)	1097-685X
ISSN	0022-5223
DOI	10.1016/j.jtcvs.2022.08.010
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Article ; Online: Orexin A attenuates palmitic acid-induced hypothalamic cell death.

Duffy, Cayla M / Nixon, Joshua P / Butterick, Tammy A

Molecular and cellular neurosciences

2016 Volume 75, Page(s) 93–100

Abstract: Palmitic acid (PA), an abundant dietary saturated fatty acid, contributes to obesity and hypothalamic dysregulation in part through increase in oxidative stress, insulin resistance, and neuroinflammation. Increased production of reactive oxygen species ( ... ...

Abstract	Palmitic acid (PA), an abundant dietary saturated fatty acid, contributes to obesity and hypothalamic dysregulation in part through increase in oxidative stress, insulin resistance, and neuroinflammation. Increased production of reactive oxygen species (ROS) as a result of PA exposure contributes to the onset of neuronal apoptosis. Additionally, high fat diets lead to changes in hypothalamic gene expression profiles including suppression of the anti-apoptotic protein B cell lymphoma 2 (Bcl-2) and upregulation of the pro-apoptotic protein B cell lymphoma 2 associated X protein (Bax). Orexin A (OXA), a hypothalamic peptide important in obesity resistance, also contributes to neuroprotection. Prior studies have demonstrated that OXA attenuates oxidative stress induced cell death. We hypothesized that OXA would be neuroprotective against PA induced cell death. To test this, we treated an immortalized hypothalamic cell line (designated mHypoA-1/2) with OXA and PA. We demonstrate that OXA attenuates PA-induced hypothalamic cell death via reduced caspase-3/7 apoptosis, stabilization of Bcl-2 gene expression, and reduced Bax/Bcl-2 gene expression ratio. We also found that OXA inhibits ROS production after PA exposure. Finally, we show that PA exposure in mHypoA-1/2 cells significantly reduces basal respiration, maximum respiration, ATP production, and reserve capacity. However, OXA treatment reverses PA-induced changes in intracellular metabolism, increasing basal respiration, maximum respiration, ATP production, and reserve capacity. Collectively, these results support that OXA protects against PA-induced hypothalamic dysregulation, and may represent one mechanism through which OXA can ameliorate effects of obesogenic diet on brain health.
Language	English
Publishing date	2016-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	1046640-x
ISSN	1095-9327 ; 1044-7431
ISSN (online)	1095-9327
ISSN	1044-7431
DOI	10.1016/j.mcn.2016.07.003
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Article: Microglial Immune Response to Low Concentrations of Combustion-Generated Nanoparticles: An In Vitro Model of Brain Health.

Duffy, Cayla M / Swanson, Jacob / Northrop, William / Nixon, Joshua P / Butterick, Tammy A

Nanomaterials (Basel, Switzerland)

2018 Volume 8, Issue 3

Abstract: The brain is the central regulator for integration and control of responses to environmental cues. Previous studies suggest that air pollution may directly impact brain health by triggering the onset of chronic neuroinflammation. We hypothesize that ... ...

Abstract	The brain is the central regulator for integration and control of responses to environmental cues. Previous studies suggest that air pollution may directly impact brain health by triggering the onset of chronic neuroinflammation. We hypothesize that nanoparticle components of combustion-generated air pollution may underlie these effects. To test this association, a microglial in vitro biological sensor model was used for testing neuroinflammatory response caused by low-dose nanoparticle exposure. The model was first validated using 20 nm silver nanoparticles (AgNP). Next, neuroinflammatory response was tested after exposure to size-selected 20 nm combustion-generated nanoparticles (CGNP) collected from a modern diesel engine. We show that low concentrations of CGNPs promote low-grade inflammatory response indicated by increased pro-inflammatory cytokine release (tumor necrosis factor-α), similar to that observed after AgNP exposure. We also demonstrate increased production of reactive oxygen species and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) p65 phosphorylation in microglia after CGNP stimulation. Finally, we show conditioned media from CGNP-stimulated microglia significantly reduced hypothalamic neuronal survival in vitro. To our knowledge, this data show for the first time that exposure to AgNP and CGNP elicits microglial neuroinflammatory response through the activation of NF-κB.
Language	English
Publishing date	2018-03-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662255-5
ISSN	2079-4991
ISSN	2079-4991
DOI	10.3390/nano8030155
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Article ; Online: Whole-body inhalation of nano-sized carbon black

Janeen H. Trembley / Simon W. So / Joshua P. Nixon / Elizabeth C. Bowdridge / Krista L. Garner / Julie Griffith / Kevin J. Engles / Thomas P. Batchelor / William T. Goldsmith / Julie M. Tomáška / Salik Hussain / Timothy R. Nurkiewicz / Tammy A. Butterick

BMC Research Notes, Vol 15, Iss 1, Pp 1-

a surrogate model of military burn pit exposure

2022 Volume 7

Abstract: Abstract Objective Chronic multisymptom illness (CMI) is an idiopathic disease affecting thousands of U.S. Veterans exposed to open-air burn pits emitting aerosolized particulate matter (PM) while serving in Central and Southwest Asia and Africa. ... ...

Abstract	Abstract Objective Chronic multisymptom illness (CMI) is an idiopathic disease affecting thousands of U.S. Veterans exposed to open-air burn pits emitting aerosolized particulate matter (PM) while serving in Central and Southwest Asia and Africa. Exposure to burn pit PM can result in profound biologic consequences including chronic fatigue, impaired cognition, and respiratory diseases. Dysregulated or unresolved inflammation is a possible underlying mechanism for CMI onset. We describe a rat model of whole-body inhalation exposure using carbon black nanoparticles (CB) as a surrogate for military burn pit-related exposure. Using this model, we measured biomarkers of inflammation in multiple tissues. Results Male Sprague Dawley rats were exposed to CB aerosols by whole body inhalation (6 ± 0.83 mg/m3). Proinflammatory biomarkers were measured in multiple tissues including arteries, brain, lung, and plasma. Biomarkers of cardiovascular injury were also assayed in plasma. CB inhalation exposure increased CMI-related proinflammatory biomarkers such as IFN-γ and TNFα in multiple tissue samples. CB exposure also induced cardiovascular injury markers (adiponectin, MCP1, sE-Selectin, sICam-1 and TIMP1) in plasma. These findings support the validity of our animal exposure model for studies of burn pit-induced CMI. Future studies will model more complex toxicant mixtures as documented at multiple burn pit sites.
Keywords	Burn Pit Exposure ; Chronic Multisymptom Illness ; Inflammation ; Cytokines ; Environmental Exposure ; Inhalation toxicology ; Medicine ; R ; Biology (General) ; QH301-705.5 ; Science (General) ; Q1-390
Subject code	610
Language	English
Publishing date	2022-08-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Microglial Immune Response to Low Concentrations of Combustion-Generated Nanoparticles

Cayla M. Duffy / Jacob Swanson / William Northrop / Joshua P. Nixon / Tammy A. Butterick

Nanomaterials, Vol 8, Iss 3, p

An In Vitro Model of Brain Health

2018 Volume 155

Abstract	The brain is the central regulator for integration and control of responses to environmental cues. Previous studies suggest that air pollution may directly impact brain health by triggering the onset of chronic neuroinflammation. We hypothesize that nanoparticle components of combustion-generated air pollution may underlie these effects. To test this association, a microglial in vitro biological sensor model was used for testing neuroinflammatory response caused by low-dose nanoparticle exposure. The model was first validated using 20 nm silver nanoparticles (AgNP). Next, neuroinflammatory response was tested after exposure to size-selected 20 nm combustion-generated nanoparticles (CGNP) collected from a modern diesel engine. We show that low concentrations of CGNPs promote low-grade inflammatory response indicated by increased pro-inflammatory cytokine release (tumor necrosis factor-α), similar to that observed after AgNP exposure. We also demonstrate increased production of reactive oxygen species and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) p65 phosphorylation in microglia after CGNP stimulation. Finally, we show conditioned media from CGNP-stimulated microglia significantly reduced hypothalamic neuronal survival in vitro. To our knowledge, this data show for the first time that exposure to AgNP and CGNP elicits microglial neuroinflammatory response through the activation of NF-κB.
Keywords	combustion-generated nanoparticles ; pollution ; microglia ; chronic inflammation ; in vitro biosensor ; neuroinflammation ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2018-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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