Outputs (16)

Thymosin beta 4 prevents systemic lipopolysaccharide-induced plaque load in middle-age APP/PS1 mice (2023)
Journal Article
Othman, O., Marshall, H., Masterson, M., Winlow, P., Gibson, G., Ding, Y., & Pardon, M. (2023). Thymosin beta 4 prevents systemic lipopolysaccharide-induced plaque load in middle-age APP/PS1 mice. International Immunopharmacology, 117, Article 109951. https://doi.org/10.1016/j.intimp.2023.109951

Lipopolysaccharide (LPS) produced by the gut during systemic infections and inflammation is thought to contribute to Alzheimer's disease (AD) progression. Since thymosin beta 4 (Tβ4) effectively reduces LPS-induced inflammation in sepsis, we tested i... Read More about Thymosin beta 4 prevents systemic lipopolysaccharide-induced plaque load in middle-age APP/PS1 mice.

Timing impairments in early Alzheimer's disease: Evidence from a mouse model (2020)
Journal Article
Armstrong, P., Pardon, M. C., & Bonardi, C. (2020). Timing impairments in early Alzheimer's disease: Evidence from a mouse model. Behavioral Neuroscience, 134(2), 82-100. https://doi.org/10.1037/bne0000359

A key characteristic of Alzheimer's disease (AD) is loss of episodic memory-memory for what happened, where and when; this final aspect-timing-is the focus of the present article. Although timing deficits have been reported in AD patients, few parall... Read More about Timing impairments in early Alzheimer's disease: Evidence from a mouse model.

Increasing Tau 4R Tau Levels Exacerbates Hippocampal Tau Hyperphosphorylation in the hTau Model of Tauopathy but Also Tau Dephosphorylation Following Acute Systemic Inflammation (2020)
Journal Article
Barron, M. R., Gartlon, J., Dawson, L. A., Atkinson, P. J., & Pardon, M. (2020). Increasing Tau 4R Tau Levels Exacerbates Hippocampal Tau Hyperphosphorylation in the hTau Model of Tauopathy but Also Tau Dephosphorylation Following Acute Systemic Inflammation. Frontiers in Immunology, 11, https://doi.org/10.3389/fimmu.2020.00293

Copyright © 2020 Barron, Gartlon, Dawson, Atkinson and Pardon. Inflammation is considered a mechanistic driver of Alzheimer's disease, thought to increase tau phosphorylation, the first step to the formation of neurofibrillary tangles (NFTs). To furt... Read More about Increasing Tau 4R Tau Levels Exacerbates Hippocampal Tau Hyperphosphorylation in the hTau Model of Tauopathy but Also Tau Dephosphorylation Following Acute Systemic Inflammation.

Transplantation of bone marrow derived macrophages reduces markers of neuropathology in an APP/PS1 mouse model (2019)
Journal Article
Costa-Marques, L., Arnold, K., Pardon, M. C., Leovsky, C., Swarbrick, S., Fabian, C., & Stolzing, A. (2019). Transplantation of bone marrow derived macrophages reduces markers of neuropathology in an APP/PS1 mouse model. Translational Neurodegeneration, 8, Article 33. https://doi.org/10.1186/s40035-019-0173-9

© 2019 The Author(s). Background: We investigated early hallmarks of putative therapeutic effects following systemic transplantation of bone marrow derived macrophages (BM-M) in APP/PS1 transgenic mice. Method: BM-M were transplanted into the tail ve... Read More about Transplantation of bone marrow derived macrophages reduces markers of neuropathology in an APP/PS1 mouse model.

Sex-specific hippocampal metabolic signatures at the onset of systemic inflammation with lipopolysaccharide in the APPswe/PS1dE9 mouse model of Alzheimer's disease (2019)
Journal Article
Agostini, A., Yuchun, D., Li, B., Kendall, D. A., & Pardon, M. (2020). Sex-specific hippocampal metabolic signatures at the onset of systemic inflammation with lipopolysaccharide in the APPswe/PS1dE9 mouse model of Alzheimer's disease. Brain, Behavior, and Immunity, 83, 87-111. https://doi.org/10.1016/j.bbi.2019.09.019

Systemic inflammation enhances the risk and progression of Alzheimer's disease (AD). Lipopolysaccharide (LPS), a potent pro-inflammatory endotoxin produced by the gut, is found in excess levels in AD where it associates with neurological hallmarks of... Read More about Sex-specific hippocampal metabolic signatures at the onset of systemic inflammation with lipopolysaccharide in the APPswe/PS1dE9 mouse model of Alzheimer's disease.

Anti-inflammatory potential of thymosin ?4 in the central nervous system: implications for progressive neurodegenerative diseases (2018)
Journal Article
Pardon, M. (2018). Anti-inflammatory potential of thymosin ?4 in the central nervous system: implications for progressive neurodegenerative diseases. Expert Opinion on Biological Therapy, 18(sup1), 165-169. https://doi.org/10.1080/14712598.2018.1486817

Introduction: The actin-sequestering thymosin beta4 (Tβ4) is the most abundant member of the β-thymosins, and is widely expressed in the central nervous system (CNS), but its functions in the healthy and diseased brain are poorly understood. The expr... Read More about Anti-inflammatory potential of thymosin ?4 in the central nervous system: implications for progressive neurodegenerative diseases.

Dynamic metabolic patterns tracking neurodegeneration and gliosis following 26S proteasome dysfunction in mouse forebrain neurons (2018)
Journal Article
Geiszler, P. C., Ugun-Klusek, A., Lawler, K., Pardon, M., Yuchun, D., Bai, L., …Bedford, L. (in press). Dynamic metabolic patterns tracking neurodegeneration and gliosis following 26S proteasome dysfunction in mouse forebrain neurons. Scientific Reports, 8, Article 4833. https://doi.org/10.1038/s41598-018-23155-2

Metabolite profiling is an important tool that may better capture the multiple features of neurodegeneration. With the considerable parallels between mouse and human metabolism, the use of metabolomics in mouse models with neurodegenerative pathology... Read More about Dynamic metabolic patterns tracking neurodegeneration and gliosis following 26S proteasome dysfunction in mouse forebrain neurons.

NAD-biosynthetic enzyme NMNAT1 reduces early behavioral impairment in the htau mouse model of tauopathy (2017)
Journal Article
Rossi, F., Geiszler, P. C., Meng, W., Barron, M., Prior, M., Herd-Smith, A., …Conforti, L. (2018). NAD-biosynthetic enzyme NMNAT1 reduces early behavioral impairment in the htau mouse model of tauopathy. Behavioural Brain Research, 339, https://doi.org/10.1016/j.bbr.2017.11.030

NAD metabolism and the NAD biosynthetic enzymes nicotinamide nucleotide adenylyltransferases (NMNATs) are thought to play a key neuroprotective role in tauopathies, including Alzheimer’s disease. Here, we investigated whether modulating the expressio... Read More about NAD-biosynthetic enzyme NMNAT1 reduces early behavioral impairment in the htau mouse model of tauopathy.

Abnormal clock gene expression and locomotor activity rhythms in two month-old female APPSwe/PS1dE9 mice (2017)
Journal Article
Oyegbami, O., Collins, H. M., Pardon, M., Ebling, F. J., Heery, D. M., & Moran, P. M. (2017). Abnormal clock gene expression and locomotor activity rhythms in two month-old female APPSwe/PS1dE9 mice. Current Alzheimer Research, 14(8), 850-860. https://doi.org/10.2174/1567205014666170317113159

In addition to cognitive decline, Alzheimer’s disease (AD) is also characterized by agitation and disruptions in activity and sleep. These symptoms typically occur in the evening or at night and have been referred to as ‘sundowning’. These symptoms a... Read More about Abnormal clock gene expression and locomotor activity rhythms in two month-old female APPSwe/PS1dE9 mice.

A state of delirium: deciphering the effect of inflammation on tau pathology in Alzheimer's disease (2016)
Journal Article
Barron, M., Gartlon, J., Dawson, L. A., Atkinson, P. J., & Pardon, M. (2017). A state of delirium: deciphering the effect of inflammation on tau pathology in Alzheimer's disease. Experimental Gerontology, 94, 103-107. https://doi.org/10.1016/j.exger.2016.12.006

Alzheimer's disease (AD), the predominant form of dementia, is highly correlated with the abnormal hyperphosphorylation and aggregation of tau. Immune responses are key drivers of AD and how they contribute to tau pathology in human disease remains l... Read More about A state of delirium: deciphering the effect of inflammation on tau pathology in Alzheimer's disease.