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235 results on '"Lipton, Jack W."'

4. Developmental exposure to the organochlorine pesticide dieldrin causes male-specific exacerbation of α-synuclein-preformed fibril-induced toxicity and motor deficits

Author

Gezer, Aysegul O., Kochmanski, Joseph, VanOeveren, Sarah E., Cole-Strauss, Allyson, Kemp, Christopher J., Patterson, Joseph R., Miller, Kathryn M., Kuhn, Nathan C., Herman, Danielle E., McIntire, Alyssa, Lipton, Jack W., Luk, Kelvin C., Fleming, Sheila M., Sortwell, Caryl E., and Bernstein, Alison I.

Published
2020
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8. Intrastriatal injection of pre-formed mouse α-synuclein fibrils into rats triggers α-synuclein pathology and bilateral nigrostriatal degeneration

Author

Paumier, Katrina L., Luk, Kelvin C., Manfredsson, Fredric P., Kanaan, Nicholas M., Lipton, Jack W., Collier, Timothy J., Steece-Collier, Kathy, Kemp, Christopher J., Celano, Stephanie, Schulz, Emily, Sandoval, Ivette M., Fleming, Sheila, Dirr, Elliott, Polinski, Nicole K., Trojanowski, John Q., Lee, Virginia M., and Sortwell, Caryl E.

Published
2015
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10. Progressive nigrostriatal terminal dysfunction and degeneration in the engrailed1 heterozygous mouse model of Parkinson's disease

Author

Nordström, Ulrika, Beauvais, Geneviève, Ghosh, Anamitra, Pulikkaparambil Sasidharan, Baby Chakrapani, Lundblad, Martin, Fuchs, Julia, Joshi, Rajiv L., Lipton, Jack W., Roholt, Andrew, Medicetty, Satish, Feinstein, Timothy N., Steiner, Jennifer A., Escobar Galvis, Martha L., Prochiantz, Alain, and Brundin, Patrik

Published
2015
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11. BDNF rs10501087, rs1491850 and rs11030094 polymorphisms associated with delayed progression in early-stage Parkinson's disease

Author

Fischer, D. Luke, Auinger, Peggy, Goudreau, John L., Paumier, Katrina L., Cole-Strauss, Allyson, Kemp, Christopher J., Lipton, Jack W., and Sortwell, Caryl E.

Subjects
Neurology, Neurology (clinical)
Abstract

Parkinson's disease (PD) is heterogenous in its presentation, progression and response to therapies. Genetic polymorphisms may account for some of this variability. Several single nucleotide polymorphisms (SNPs) in the brain-derived neurotrophic factor gene BDNF have been associated with differing clinical outcomes from different dopaminergic replacement strategies, and one of these, the rs6265 SNP, has been associated with a milder clinical phenotype in the unmedicated, early-stage of PD. We examined if other BDNF SNPs with potential pharmacogenetic effects also are associated with different rates of disease progression. The Deprenyl And Tocopherol Antioxidative Therapy Of Parkinsonism (DATATOP) study was analyzed retrospectively. DNA samples (n = 217) were genotyped for the BDNF rs908867, rs11030094, rs10501087, rs1157659, and rs1491850 SNPs, and the primary endpoint was time to initiate symptomatic pharmacotherapy. Genotypes were compared using the Cox proportional hazard ratio (HR) with baseline age, sex, site, time since PD diagnosis and rs6265 genotype as covariates. The primary endpoint was associated with a delay with three SNPs: rs10501087 [HR (95% Confidence Interval) = 28.3 (3.6–223.1, p = 0.002) and 7.6 (1.9–29.8, p = 0.004) for T/T and T/C subjects, respectively, vs. C/C subjects], rs1491850 [HR = 3.3 (1.3–8.4, p = 0.04) and 2.8 (1.3–6.4, p = 0.03) for T/T and T/C subjects, respectively, vs. C/C subjects] and rs11030094 [HR = 2.5 (1.1–5.6, p = 0.03) and 2.0 (1.3–6.4, p = 0.03) for A/A and A/G subjects, respectively, vs. G/G subjects]. From the primary endpoint, specific rs10501087, rs1491850, and rs11030094 SNP genotypes are associated with a slower rate of PD progression in the unmedicated state. A prospective clinical trial examining many BDNF SNPs is warranted.

Published
2022
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18. Large-Scale SARS-CoV-2 Testing Utilizing Saliva and Transposition Sample Pooling

Author

Patterson, Joseph R., primary, Cole-Strauss, Allyson, primary, Kuhn, Nathan, primary, Mercier, Carlene, primary, Kochmanski, Joseph, primary, Gerlach, John A., primary, LeVeque, Rhiannon M., primary, Neugebauer, Kerri A., primary, Conner, Kayla N., primary, Gomez, Jasper, primary, Hennes, Mark G., primary, Thompson, Kaje’ne E., primary, Rytlewski, Destinee L., primary, Bigwood, Chloe C., primary, Scharmen, Amy, primary, Simjanovski, Gabriel, primary, Riley, Cassidy, primary, Donaldson, Jessica, primary, Yasin, Dilann, primary, Kouja, Najwa, primary, Contejean, Zaria, primary, Burnett, Michaela, primary, Aminova, Shakhlo, primary, Yawson, Nat Ato, primary, Singh, Simran B., primary, Alian, Osama M., primary, Broeker, Carson D., primary, Zaluzec, Erin K., primary, ONeill, Morgan, primary, Puschner, Birgit, primary, Sousa, Aron, primary, Bix, Laura, primary, Jespersen, Brian, primary, Holzman, Claudia, primary, Mitchell, Jade, primary, Julien, Ryan, primary, Askin, Yesim, primary, Barnes, Danielle, primary, Durshanpalli, Purna, primary, Krum, Doug, primary, Weber, Rett, primary, Patterson, Morgan, primary, Anderson, Becky, primary, Hunt, Ryan, primary, O’Brien, Benjamin, primary, Umstead, Andrew, primary, Beck, John S., primary, Vega, Irving E., primary, Sortwell, Caryl E., primary, and Lipton, Jack W., primary

Published
2022
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30. Subthalamic Nucleus Stimulation Increases Brain Derived Neurotrophic Factor in the Nigrostriatal System and Primary Motor Cortex

Author

Steece-Collier, Kathy, Behbehani, Michael M., Collier, Timothy J., Wohlgenant, Susan L., Kemp, Christopher J., Cole-Strauss, Allyson, Levine, Nathan D., Lipton, Jack W., and Sortwell, Caryl E.

Abstract

The mechanisms underlying the effects of long-term deep brain stimulation of the subthalamic nucleus (STN DBS) as a therapy for Parkinson's disease (PD) remain poorly understood. The present study examined whether functionally effective, long-term STN DBS modulates glial cell line-derived neurotrophic factor (GDNF) and/or brain-derived neurotrophic factor (BDNF) in both unlesioned and unilateral 6-hydroxydopamine lesioned rats. Lesioned rats that received two weeks of continuous unilateral STN DBS exhibited significant improvements in parkinsonian motor behaviors in tests of forelimb akinesia and rearing activity. Unilateral STN DBS did not increase GDNF in the nigrostriatal system, primary motor cortex (M1), or hippocampus of unlesioned rats. In contrast, unilateral STN DBS increased BDNF protein 2–3 fold bilaterally in the nigrostriatal system with the location (substantia nigra vs. striatum) dependent upon lesion status. Further, BDNF protein was bilaterally increased in M1 cortex by as much as 2 fold regardless of lesion status. STN DBS did not impact cortical regions that receive less input from the STN. STN DBS also was associated with bilateral increases in BDNF mRNA in the substantia nigra (SN) and internal globus pallidus (GPi). The increase observed in GPi was completely blocked by pretreatment with 5-Methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine (MK-801), suggesting that the activation of N-methyl-D-aspartate (NMDA) receptors was involved in this phenomenon. The upregulation of BDNF associated with long term STN DBS suggest that this therapy may exert pronounced and underappreciated effects on plasticity in the basal ganglia circuitry that may play a role in the symptomatic effects of this therapy as well as support the neuroprotective effect of stimulation documented in this rat model.

Published
2022
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31. BDNFrs6265 Genotype Influences Outcomes of Pharmacotherapy and Subthalamic Nucleus Deep Brain Stimulation in Early-Stage Parkinson's Disease

Author

Sortwell, Caryl E., Hacker, Mallory L., Fischer, David Luke, Konrad, Peter E., Davis, Thomas L., Neimat, Joseph S., Wang, Lily, Song, Yanna, Mattingly, Zach R., Cole-Strauss, Allyson, Lipton, Jack W., and Charles, P. David

Abstract

The efficacy of pharmacotherapy and deep brain stimulation of the subthalamic nucleus in treating Parkinson's disease motor symptoms is highly variable and may be influenced by patient genotype. The relatively common (prevalence about one in three) and protein-altering rs6265 single nucleotide polymorphism (C > T) in the gene BDNFhas been associated with different clinical outcomes with levodopa.

Published
2022
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35. Developmental exposure to the organochlorine pesticide dieldrin causes male-specific exacerbation of α-synuclein-preformed fibril-induced toxicity and motor deficits

Author

Gezer, Aysegul O., primary, Kochmanski, Joseph, additional, VanOeveren, Sarah E., additional, Cole-Strauss, Allyson, additional, Kemp, Christopher J, additional, Patterson, Joseph R., additional, Miller, Kathryn M., additional, Kuhn, Nathan C., additional, Herman, Danielle E., additional, McIntire, Alyssa, additional, Lipton, Jack W., additional, Luk, Kelvin C., additional, Fleming, Sheila M., additional, Sortwell, Caryl E., additional, and Bernstein, Alison I., additional

Published
2020
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43. Subthalamic Nucleus Deep Brain Stimulation Does Not Modify the Functional Deficits or Axonopathy Induced by Nigrostriatal α-Synuclein Overexpression

Author

Fischer, D. Luke, primary, Manfredsson, Fredric P., additional, Kemp, Christopher J., additional, Cole-Strauss, Allyson, additional, Lipton, Jack W., additional, Duffy, Megan F., additional, Polinski, Nicole K., additional, Steece-Collier, Kathy, additional, Collier, Timothy J., additional, Gombash, Sara E., additional, Buhlinger, Daniel J., additional, and Sortwell, Caryl E., additional

Published
2017
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45. Parkinson's disease-linked D620N VPS35 knockin mice manifest tau neuropathology and dopaminergic neurodegeneration.

Author

Xi Chen, Kordich, Jennifer K., Williams, Erin T., Levine, Nathan, Cole-Strauss, Allyson, Marshall, Lee, Labrie, Viviane, Jiyan Ma, Lipton, Jack W., and Moore, Darren J.

Subjects
PROTEINS, GENE expression, PARKINSON'S disease, GENETIC mutation, NEURODEGENERATION
Abstract

Mutations in the vacuolar protein sorting 35 ortholog (VPS35) gene represent a cause of late-onset, autosomal dominant familial Parkinson's disease (PD). A single missense mutation, D620N, is considered pathogenic based upon its segregation with disease in multiple families with PD. At present, the mechanism(s) by which familial VPS35 mutations precipitate neurodegeneration in PD are poorly understood. Here, we employ a germline D620N VPS35 knockin (KI) mouse model of PD to formally establish the age-related pathogenic effects of the D620N mutation at physiological expression levels. Our data demonstrate that a heterozygous or homozygous D620N mutation is sufficient to reproduce key neuropathological hallmarks of PD as indicated by the progressive degeneration of nigrostriatal pathway dopaminergic neurons and widespread axonal pathology. Unexpectedly, endogenous D620N VPS35 expression induces robust tau-positive somatodendritic pathology throughout the brain as indicated by abnormal hyperphosphorylated and conformation-specific tau, which may represent an important and early feature of mutant VPS35-induced neurodegeneration in PD. In contrast, we find no evidence for α-synuclein-positive neuropathology in aged VPS35 KI mice, a hallmark of Lewy body pathology in PD. D620N VPS35 expression also fails to modify the lethal neurodegenerative phenotype of human A53T-a-synuclein transgenic mice. Finally, by crossing VPS35 KI and null mice, our data demonstrate that a single D620N VPS35 allele is sufficient for survival and early maintenance of dopaminergic neurons, indicating that the D620N VPS35 protein is fully functional. Our data raise the tantalizing possibility of a pathogenic interplay between mutant VPS35 and tau for inducing neurodegeneration in PD. [ABSTRACT FROM AUTHOR]

Published
2019
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49. The Longitudinal Transcriptomic Response of the Substantia Nigra to Intrastriatal 6-Hydroxydopamine Reveals Significant Upregulation of Regeneration-Associated Genes

Author

Kanaan, Nicholas M., primary, Collier, Timothy J., additional, Cole-Strauss, Allyson, additional, Grabinski, Tessa, additional, Mattingly, Zachary R., additional, Winn, Mary E., additional, Steece-Collier, Kathy, additional, Sortwell, Caryl E., additional, Manfredsson, Fredric P., additional, and Lipton, Jack W., additional

Published
2015
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