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31 results on '"Meyerdirk, Lindsay"'

3. Urinary tract infections trigger synucleinopathy via the innate immune response

Author

Peelaerts, Wouter, Mercado, Gabriela, George, Sonia, Villumsen, Marie, Kasen, Alysa, Aguileta, Miguel, Linstow, Christian, Sutter, Alexandra B., Kuhn, Emily, Stetzik, Lucas, Sheridan, Rachel, Bergkvist, Liza, Meyerdirk, Lindsay, Lindqvist, Allison, Gavis, Martha L. Escobar, Van den Haute, Chris, Hultgren, Scott J., Baekelandt, Veerle, Pospisilik, J. Andrew, Brudek, Tomasz, Aznar, Susana, Steiner, Jennifer A., Henderson, Michael X., Brundin, Lena, Ivanova, Magdalena I., Hannan, Tom J., and Brundin, Patrik

Published
2023
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4. Air pollution nanoparticle and alpha-synuclein fibrils synergistically decrease glutamate receptor A1, depending upon nPM batch activity

Author

Zhang, Hongqiao, D'Agostino, Carla, Tulisiak, Christopher, Thorwald, Max A., Bergkvist, Liza, Lindquist, Allison, Meyerdirk, Lindsay, Schulz, Emily, Becker, Katelyn, Steiner, Jennifer A., Cacciottolo, Mafalda, Kwatra, Mohit, Rey, Nolwen L., Escobar Galvis, Martha L., Ma, Jiyan, Sioutas, Constantinos, Morgan, Todd E., Finch, Caleb E., and Brundin, Patrik

Published
2023
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5. Human Endogenous Retrovirus Expression is Dynamically Regulated in Parkinson’s Disease

Author

Gordevičius, Juozas, primary, Goralski, Thomas, additional, Bergsma, Alexis, additional, Parham, Andrea, additional, Kuhn, Emily, additional, Meyerdirk, Lindsay, additional, McDonald, Mitch, additional, Milčiūtė, Milda, additional, Putten, Elizabeth Van, additional, Marshall, Lee, additional, Brundin, Patrik, additional, Brundin, Lena, additional, Labrie, Viviane, additional, Henderson, Michael, additional, and Pospisilik, John Andrew, additional

Published
2023
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11. A novel automated morphological analysis of Iba1+ microglia using a deep learning assisted model

Author

Stetzik, Lucas, primary, Mercado, Gabriela, additional, Smith, Lindsey, additional, George, Sonia, additional, Quansah, Emmanuel, additional, Luda, Katarzyna, additional, Schulz, Emily, additional, Meyerdirk, Lindsay, additional, Lindquist, Allison, additional, Bergsma, Alexis, additional, Jones, Russell G., additional, Brundin, Lena, additional, Henderson, Michael X., additional, Pospisilik, John Andrew, additional, and Brundin, Patrik, additional

Published
2022
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12. Synaptic location is a determinant of the detrimental effects of α-synuclein pathology to glutamatergic transmission in the basolateral amygdala

Author

Chen, Liqiang, primary, Nagaraja, Chetan, primary, Daniels, Samuel, primary, Fisk, Zoe A, additional, Dvorak, Rachel, additional, Meyerdirk, Lindsay, additional, Steiner, Jennifer A, additional, Escobar Galvis, Martha L, additional, Henderson, Michael X, additional, Rousseaux, Maxime WC, additional, Brundin, Patrik, additional, and Chu, Hong-Yuan, additional

Published
2022
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13. Author response: Synaptic location is a determinant of the detrimental effects of α-synuclein pathology to glutamatergic transmission in the basolateral amygdala

Author

Chen, Liqiang, primary, Nagaraja, Chetan, primary, Daniels, Samuel, primary, Fisk, Zoe A, additional, Dvorak, Rachel, additional, Meyerdirk, Lindsay, additional, Steiner, Jennifer A, additional, Escobar Galvis, Martha L, additional, Henderson, Michael X, additional, Rousseaux, Maxime WC, additional, Brundin, Patrik, additional, and Chu, Hong-Yuan, additional

Published
2022
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14. A novel automated morphological analysis of microglia activation using a deep learning assisted model

Author

Stetzik Lucas, Mercado Gabriela, Smith Lindsey, George Sonia, Quansah Emmanuel, Luda Katarzyna, Schulz Emily, Meyerdirk Lindsay, Lindquist Allison, Bergsma Alexis, Russell G Jones, Brundin Lena, Michael X Henderson, Pospisilik John Andrew, and Brundin Patrik

Abstract

There is growing evidence for the key role of microglial activation in brain pathophysiology. Consequently, there is a need for efficient automated methods to measure the morphological changes distinctive of microglia functional states in research settings. Currently, many commonly used automated methods can be subject to sample representation bias, time consuming imaging, specific hardware requirements, and difficulty in maintaining an accurate comparison across research environments. To overcome these issues, we use commercially available deep learning tools (Aiforia® Cloud (Aifoira Inc., Cambridge, United States) to quantify microglial morphology and cell counts from histopathological slides of Iba1 stained tissue sections. We provide evidence for the effective application of this method across a range of independently collected datasets in mouse models of viral infection and Parkinson’s disease. Additionally, we provide a comprehensive workflow with training details and annotation strategies by feature layer that can be used as a guide to generate new models. In addition, all models described in this work are shared within the Aiforia® platform and are available for study-specific adaptation and validation.

Published
2022

15. Air Pollution Nanoparticle and Alpha-Synuclein Fibrils Synergistically Decrease Glutamate Receptor A1, Depending Upon NPM Batch Activity

Author

Zhang, Hongqiao, primary, D'Agostino, Carla, additional, Tulisiak, Christopher, additional, Thorwald, Max, additional, Bergkvist, Liza, additional, Lindquist, Allison, additional, Meyerdirk, Lindsay, additional, Schulz, Emily, additional, Becker, Katelyn, additional, Steiner, Jennifer, additional, Cacciottolo, Mafalda, additional, Kwatra, Mohit, additional, Rey, Nolwen, additional, Escobar Galvis, Martha, additional, Ma, Jiyan, additional, Sioutas, Constantinos, additional, Morgan, Todd, additional, Finch, Caleb E, additional, and Brundin, Patrik, additional

Published
2022
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16. Heterozygous GBA D409V and ATP13a2 mutations do not exacerbate pathological α-synuclein spread in the prodromal preformed fibrils model in young mice

Author

Johnson, Michaela E., primary, Bergkvist, Liza, additional, Stetzik, Lucas, additional, Steiner, Jennifer A., additional, Meyerdirk, Lindsay, additional, Schulz, Emily, additional, Wolfrum, Emily, additional, Luk, Kelvin C., additional, Wesson, Daniel W., additional, Krainc, Dimitri, additional, and Brundin, Patrik, additional

Published
2021
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19. T Cells Limit Accumulation of Aggregate Pathology Following Intrastriatal Injection of α-Synuclein Fibrils

Author

George, Sonia, primary, Tyson, Trevor, additional, Rey, Nolwen L., additional, Sheridan, Rachael, additional, Peelaerts, Wouter, additional, Becker, Katelyn, additional, Schulz, Emily, additional, Meyerdirk, Lindsay, additional, Burmeister, Amanda R., additional, von Linstow, Christian U., additional, Steiner, Jennifer A., additional, Galvis, Martha L. Escobar, additional, Ma, Jiyan, additional, Pospisilik, J. Andrew, additional, Labrie, Viviane, additional, Brundin, Lena, additional, and Brundin, Patrik, additional

Published
2021
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20. Inhibiting the mitochondrial pyruvate carrier does not ameliorate synucleinopathy in the absence of inflammation or metabolic deficits

Author

Peelaerts, Wouter, primary, Bergkvist, Liza, additional, George, Sonia, additional, Johnson, Michaela, additional, Meyerdirk, Lindsay, additional, Ku, Emily, additional, Steiner, Jennifer A., additional, Madaj, Zachary, additional, Ma, Jiyan, additional, Becker, Katelyn, additional, Nilsson, K. Peter R., additional, Colca, Jerry, additional, and Brundin, Patrik, additional

Published
2020
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22. T cells limit accumulation of aggregate pathology following intrastriatal injection of α-synuclein fibrils

Author

George, Sonia, primary, Tyson, Trevor, additional, Rey, Nolwen L., additional, Sheridan, Rachael, additional, Peelaerts, Wouter, additional, Becker, Katelyn, additional, Schulz, Emily, additional, Meyerdirk, Lindsay, additional, Burmeister, Amanda R., additional, Steiner, Jennifer A., additional, Escobar Galvis, Martha L., additional, Ma, Jiyan, additional, Pospisilik, Andrew, additional, Labrie, Viviane, additional, Brundin, Lena, additional, and Brundin, Patrik, additional

Published
2020
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24. Metabolomic Profiling of Bile Acids in an Experimental Model of Prodromal Parkinson’s Disease

Author

Graham, Stewart, primary, Rey, Nolwen, additional, Ugur, Zafer, additional, Yilmaz, Ali, additional, Sherman, Eric, additional, Maddens, Michael, additional, Bahado-Singh, Ray, additional, Becker, Katelyn, additional, Schulz, Emily, additional, Meyerdirk, Lindsay, additional, Steiner, Jennifer, additional, Ma, Jiyan, additional, and Brundin, Patrik, additional

Published
2018
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25. Biochemical Profiling of the Brain and Blood Metabolome in a Mouse Model of Prodromal Parkinson’s Disease Reveals Distinct Metabolic Profiles

Author

Graham, Stewart F., primary, Rey, Nolwen L., additional, Yilmaz, Ali, additional, Kumar, Praveen, additional, Madaj, Zachary, additional, Maddens, Michael, additional, Bahado-Singh, Ray O., additional, Becker, Katelyn, additional, Schulz, Emily, additional, Meyerdirk, Lindsay K., additional, Steiner, Jennifer A., additional, Ma, Jiyan, additional, and Brundin, Patrik, additional

Published
2018
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30. Spatial transcriptomics reveals molecular dysfunction associated with Lewy pathology.

Author

Goralski T, Meyerdirk L, Breton L, Brasseur L, Kurgat K, DeWeerd D, Turner L, Becker K, Adams M, Newhouse D, and Henderson MX

Abstract

Lewy pathology composed of α-synuclein is the key pathological hallmark of Parkinson's disease (PD), found both in dopaminergic neurons that control motor function, and throughout cortical regions that control cognitive function. Recent work has investigated which dopaminergic neurons are most susceptible to death, but little is known about which neurons are vulnerable to developing Lewy pathology and what molecular changes an aggregate induces. In the current study, we use spatial transcriptomics to selectively capture whole transcriptome signatures from cortical neurons with Lewy pathology compared to those without pathology in the same brains. We find, both in PD and in a mouse model of PD, that there are specific classes of excitatory neurons that are vulnerable to developing Lewy pathology in the cortex. Further, we identify conserved gene expression changes in aggregate-bearing neurons that we designate the Lewy-associated molecular dysfunction from aggregates (LAMDA) signature. This gene signature indicates that neurons with aggregates downregulate synaptic, mitochondrial, ubiquitin-proteasome, endo-lysosomal, and cytoskeletal genes and upregulate DNA repair and complement/cytokine genes. However, beyond DNA repair gene upregulation, we find that neurons also activate apoptotic pathways, suggesting that if DNA repair fails, neurons undergo programmed cell death. Our results identify neurons vulnerable to Lewy pathology in the PD cortex and identify a conserved signature of molecular dysfunction in both mice and humans., Competing Interests: COMPETING INTERESTS The authors declare no competing interests.

Published
2023
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31. Inhibiting the mitochondrial pyruvate carrier does not ameliorate synucleinopathy in the absence of inflammation or metabolic deficits.

Author

Peelaerts W, Bergkvist L, George S, Johnson M, Meyerdirk L, Schulz E, Steiner JA, Madaj Z, Ma J, Becker K, Nilsson KPR, Colca JR, and Brundin P

Abstract

Epidemiological studies suggest a link between type-2 diabetes and Parkinson's disease (PD) risk. Treatment of type-2 diabetes with insulin sensitizing drugs lowers the risk of PD. We previously showed that the insulin sensitizing drug, MSDC-0160, ameliorates pathogenesis in some animal models of PD. MSDC-0160 reversibly binds the mitochondrial pyruvate carrier (MPC) protein complex, which has an anti-inflammatory effect and restores metabolic deficits. Since PD is characterized by the deposition of α-synuclein (αSyn), we hypothesized that inhibiting the MPC might directly inhibit αSyn aggregation in vivo in mammals. To answer if modulation of MPC can reduce the development of αSyn assemblies, and reduce neurodegeneration, we treated two chronic and progressive mouse models; a viral vector-based αSyn overexpressing model and a pre-formed fibril (PFF) αSyn seeding model with MSDC-0160. These two models present distinct types of αSyn pathology but lack inflammatory or autophagy deficits. Contrary to our hypothesis, we found that a modulation of MPC in these models did not reduce the accumulation of αSyn aggregates or mitigate neurotoxicity. Instead, MSDC-0160 changed the post-translational modification and aggregation features of αSyn. These results are consistent with the lack of a direct effect of MPC modulation on synuclein clearance in these models.

Published
2020
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