Researchers cited MBF Bioscience systems in 27 papers between 3/23/2018 and 4/6/2018

Stereo Investigator: 
Crupi, R., Impellizzeri, D., Cordaro, M., Siracusa, R., Casili, G., Evangelista, M., & Cuzzocrea, S. (2018). N-palmitoylethanolamide Prevents Parkinsonian Phenotypes in Aged Mice.  Molecular Neurobiology. doi: 10.1007/s12035-018-0959-2.

Dingle, A. M., Yap, K. K., Gerrand, Y.-W., Taylor, C. J., Keramidaris, E., Lokmic, Z., . . . Mitchell, G. M. (2018). Characterization of isolated liver sinusoidal endothelial cells for liver bioengineering. Angiogenesis. doi: 10.1007/s10456-018-9610-0.

Duthie, M. S., Pena, M. T., Ebenezer, G. J., Gillis, T. P., Sharma, R., Cunningham, K., . . . Reed, S. G. (2018). LepVax, a defined subunit vaccine that provides effective pre-exposure and post-exposure prophylaxis of M. leprae infection. npj Vaccines, 3(1), 12. doi: 10.1038/s41541-018-0050-z.

Dutta, R. R., Taffe, M. A., & Mandyam, C. D. (2018). Chronic administration of amphetamines disturbs development of neural progenitor cells in young adult nonhuman primates. Progress in Neuro-Psychopharmacology and Biological Psychiatry. doi: https://doi.org/10.1016/j.pnpbp.2018.03.023.

Hormigo, S., López, D. E., Cardoso, A., Zapata, G., Sepúlveda, J., & Castellano, O. (2018). Direct and indirect nigrofugal projections to the nucleus reticularis pontis caudalis mediate in the motor execution of the acoustic startle reflex. Brain Structure and Function. doi: 10.1007/s00429-018-1654-9.

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Researchers cited MBF Bioscience systems in 13 papers between 3/16/2018 and 3/23/2018

Stereo Investigator:
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Cisbani, G., Le Behot, A., Plante, M.-M., Préfontaine, P., Lecordier, M., & Rivest, S. (2018). Role of the chemokine receptors CCR2 and CX3CR1 in an experimental model of thrombotic stroke. Brain, Behavior, and Immunity. doi: https://doi.org/10.1016/j.bbi.2018.03.008.

Du, R.-H., Sun, H.-B., Hu, Z.-L., Lu, M., Ding, J.-H., & Hu, G. (2018). Kir6.1/K-ATP channel modulates microglia phenotypes: implication in Parkinson’s disease. Cell death & disease, 9(3), 404. doi: 10.1038/s41419-018-0437-9.

McGowan, S. E., & McCoy, D. M. (2018). Neuropilin-1and platelet-derived growth factor receptors cooperatively regulate intermediate filaments and mesenchymal cell migration during alveolar septation. American Journal of Physiology-Lung Cellular and Molecular Physiology.

Nagahara, A. H., Wilson, B. R., Ivasyk, I., Kovacs, I., Rawalji, S., Bringas, J. R., . . . Bankiewicz, K. S. (2018). MR-guided delivery of AAV2-BDNF into the entorhinal cortex of non-human primates. Gene Therapy, 1.

Neurolucida:

Brudvig, J. J., Cain, J. T., Schmidt-Grimminger, G. G., Stumpo, D. J., Roux, K. J., Blackshear, P. J., & Weimer, J. M. (2018). MARCKS Is Necessary for Netrin-DCC Signaling and Corpus Callosum Formation.  Molecular Neurobiology. doi: 10.1007/s12035-018-0990-3.

Carr, H., Alexander, T. C., Groves, T., Kiffer, F., Wang, J., Price, E., . . . Allen, A. R. (2018). Early effects of 16O radiation on Neuronal Morphology and Cognition in a Murine Model. Life Sciences in Space Research. doi: https://doi.org/10.1016/j.lssr.2018.03.001Continue reading “Researchers cited MBF Bioscience systems in 13 papers between 3/16/2018 and 3/23/2018” »

Researchers cited MBF Bioscience systems in 11 papers between 3/9/2018 and 3/16/2018

Stereo Investigator:
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Deroche-Gamonet, V., Revest, J.-M., Fiancette, J.-F., Balado, E., Koehl, M., Grosjean, N., . . . Piazza, P.-V. (2018). Depleting adult dentate gyrus neurogenesis increases cocaine-seeking behavior. Molecular Psychiatry. doi: 10.1038/s41380-018-0038-0.

Mendez-Gomez, H. R., Singh, J., Meyers, C., Chen, W., Gorbatyuk, O. S., & Muzyczka, N. (2018). The Lipase Activity of Phospholipase D2 is Responsible for Nigral Neurodegeneration in a Rat Model of Parkinson’s Disease. Neuroscience. doi: https://doi.org/10.1016/j.neuroscience.2018.02.047.

Wang, Y., Wang, Y., Liu, J., & Wang, X. (2018). Electroacupuncture Alleviates Motor Symptoms and Up-Regulates Vesicular Glutamatergic Transporter 1 Expression in the Subthalamic Nucleus in a Unilateral 6-Hydroxydopamine-Lesioned Hemi-Parkinsonian Rat Model.  Neuroscience bulletin. doi: 10.1007/s12264-018-0213-y.

Neurolucida:

Borreca, A., Latina, V., Corsetti, V., Middei, S., Piccinin, S., Della Valle, F., . . . Amadoro, G. (2018). AD-Related N-Terminal Truncated Tau Is Sufficient to Recapitulate In Vivo the Early Perturbations of Human Neuropathology: Implications for Immunotherapy. Molecular Neurobiology. doi: 10.1007/s12035-018-0974-3.

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Researchers cited MBF Bioscience systems in 28 papers between 3/2/2018 and 3/9/2018

Stereo Investigator:
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Akca, G., Eren, H., Tumkaya, L., Mercantepe, T., Horsanali, M. O., Deveci, E., . . . Yilmaz, A. (2018). The protective effect of astaxanthin against cisplatin-induced nephrotoxicity in rats. Biomedicine and Pharmacotherapy, 100, 575-582. doi: https://doi.org/10.1016/j.biopha.2018.02.042.

Aytan, N., Choi, J.-K., Carreras, I., Crabtree, L., Nguyen, B., Lehar, M., . . . Dedeoglu, A. Protective effects of 7,8-dihydroxyflavone on neuropathological and neurochemical changes in a mouse model of Alzheimer’s disease. European Journal of Pharmacology. doi: https://doi.org/10.1016/j.ejphar.2018.02.045.

Chu, X., Zhou, S., Sun, R., Wang, L., Xing, C., Liang, R., & Kong, Q. (2018). Chrysophanol Relieves Cognition Deficits and Neuronal Loss Through Inhibition of Inflammation in Diabetic Mice. Neurochemical Research. doi: 10.1007/s11064-018-2503-1. https://doi.org/10.1007/s11064-018-2503-1

Domínguez-Álvaro, M., Montero-Crespo, M., Blazquez-Llorca, L., Insausti, R., DeFelipe, J., & Alonso-Nanclares, L. (2018). Three-dimensional analysis of synapses in the transentorhinal cortex of Alzheimer’s disease patients. Acta Neuropathologica Communications, 6(1), 20. doi: 10.1186/s40478-018-0520-6.

El Massri, N., Weinrich, T. W., Kam, J. H., Jeffery, G., & Mitrofanis, J. (2018). Photobiomodulation reduces gliosis in the basal ganglia of aged mice. Neurobiology of Aging. doi: https://doi.org/10.1016/j.neurobiolaging.2018.02.019.

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Diet Restriction Slows Neurodegeneration and Extends Lifespan of DNA-Repair-Deficient Mice

DNA damage occurs in human cells at a constant rate. These cells are usually able to repair themselves, but sometimes deficiencies in certain genes cause the repair process to shut down. When damaged DNA isn’t fixed, mutations can occur that cause accelerated aging or cancerous tumors to form (Hoeijmakers, 2009). Scientists at Erasmus University Medical Center in Rotterdam have found a way to slow down the process – at least in mice.

In a study published in Nature, the researchers report that when mice deficient in the DNA-repair genes Ercc1 or Xpg are put on a restricted diet, they experience better overall health and increased lifespans compared to DNA-repair-deficient mice fed a normal diet. They also found significantly lower levels of neurodegeneration in the brains and spinal cords of diet restricted animals compared to controls.

“Here we report that a dietary restriction of 30 percent tripled the median and maximal remaining lifespans of these progeroid mice, strongly retarding numerous aspects of accelerated aging Mice undergoing dietary restriction retained 50 percent more neurons and maintained full motor function far beyond the lifespan of mice fed ad libitum,” (Vermeij, et al 2016).

Since the DNA-repair-deficient mice were already smaller and weaker than normal mice, the Rotterdam researchers wondered whether diet restriction would be beneficial or detrimental to their health. They found that gradually restricting the diets of DNA-repair-deficient mice starting at age seven weeks increased their median lifespans from 10 to 35 weeks in males and 13 to 39 weeks in females as compared to controls.

They also saw significant differences in the levels of neurodegeneration between these two populations. Using Stereo Investigator, they found 50 percent more neurons in the brains of diet-restricted mice compared to those fed a normal diet. They also saw lower levels of cells expressing p53 – a protein expressed in response to DNA damage – in diet-restricted mice.

According to the authors, dietary restriction may not fix defects in DNA repair mechanisms, but it may help to reduce the severity and speed at which the damage occurs.

“Our findings establish the Ercc1 mouse as a powerful model organism for health-sustaining interventions, reveal potential for reducing endogenous DNA damage, facilitate a better understanding of the molecular mechanism of dietary restriction and suggest a role for counterintuitive dietary-restriction-like therapy for human progeroid genome instability syndromes and possibly neurodegeneration in general,” (Vermeij, et al 2016).

Vermeij W.P., Dollé M.E.T., Reiling E., Jaarsma D., Payan-Gomez C, Bombardieri C.R., Wu H., Roks A.J.M., Botter S.M., van der Eerden B.C., Youssef S.A., Kuiper R.V., Nagarajah B., van Oostrom C.T., Brandt R.M.C., Barnhoorn S., Imholz S., Pennings J.L.A., de Bruin A., Gyenis Á., Pothof J, Vijg J, van Steeg H., and Hoeijmakers J.H.J. (2016) Restricted diet delays accelerated aging and genomic stress in DNA repair deficient mice. Nature 537, 427-431, doi:10.1038/nature19329

Hoeijmakers JH (2009) DNA Damage, aging, and cancer. N Engl J Med; 361:1475-1485, DOI: 10.1056/NEJMra0804615

Stock image of DNA used in accordance with the CC0 public domain license.

Researchers cited MBF systems in 27 papers between 3/20/2017 and 3/30/2017

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Abe, C., Inoue, T., Inglis, M. A., Viar, K. E., Huang, L., Ye, H., . . . Guyenet, P. G. (2017). C1 neurons mediate a stress-induced anti-inflammatory reflex in mice. Nature Neuroscience, advance online publication. doi: 10.1038/nn.4526

Caldwell, A. S. L., Edwards, M. C., Desai, R., Jimenez, M., Gilchrist, R. B., Handelsman, D. J., & Walters, K. A. (2017). Neuroendocrine androgen action is a key extraovarian mediator in the development of polycystic ovary syndrome. Proceedings of the National Academy of Sciences. doi: 10.1073/pnas.1616467114.

Castro-Hernández, J., Adlard, P. A., & Finkelstein, D. I. (2017). Pramipexole restores depressed transmission in the ventral hippocampus following MPTP-lesion. Scientific Reports, 7, 44426. doi: 10.1038/srep44426.

Dawes, W. J., Zhang, X., Fancy, S. P., Rowitch, D., & Marino, S. (2017). Moderate-Grade Germinal Matrix Haemorrhage Activates Cell Division in the Neonatal Mouse Subventricular Zone. Developmental Neuroscience.

Drobyshevsky, A., & Quinlan, K. A. (2017). Spinal cord injury in hypertonic newborns after antenatal hypoxia-ischemia in a rabbit model of cerebral palsy. Experimental Neurology, 293, 13-26. doi: http://dx.doi.org/10.1016/j.expneurol.2017.03.017.

El Massri, N., Lemgruber, A. P., Rowe, I. J., Moro, C., Torres, N., Reinhart, F., . . . Mitrofanis, J. (2017). Photobiomodulation-induced changes in a monkey model of Parkinson’s disease: changes in tyrosine hydroxylase cells and GDNF expression in the striatum. Experimental Brain Research, 1-14. doi: 10.1007/s00221-017-4937-0.

Hühner, L., Rilka, J., Gilsbach, R., Zhou, X., Machado, V., & Spittau, B. (2017). Interleukin-4 Protects Dopaminergic Neurons In vitro but Is Dispensable for MPTP-Induced Neurodegeneration In vivo. Frontiers in Molecular Neuroscience, 10(62). doi: 10.3389/fnmol.2017.00062.

Meng, L., Huang, T., Sun, C., Hill, D. L., & Krimm, R. (2017). BDNF is required for taste axon regeneration following unilateral chorda tympani nerve section. Experimental Neurology, 293, 27-42. doi: http://dx.doi.org/10.1016/j.expneurol.2017.03.016.

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Researchers cited MBF systems in 28 papers during the week of 03/06/2017

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Akkhawattanangkul, Y., Maiti, P., Xue, Y., Aryal, D., Wetsel, W. C., Hamilton, D., . . . McDonald, M. P. (2017). Targeted deletion of GD3 synthase protects against MPTP-induced neurodegeneration. Genes, Brain and Behavior, n/a-n/a. doi: 10.1111/gbb.12377.

Chung, Y. C., Baek, J. Y., Kim, S. R., Ko, H. W., Bok, E., Shin, W.-H., . . . Jin, B. K. (2017). Capsaicin prevents degeneration of dopamine neurons by inhibiting glial activation and oxidative stress in the MPTP model of Parkinson/’s disease. Experimental and Molecular Medicine, 49, e298. doi: 10.1038/emm.2016.159.

Hajheidari, S., Sameni, H. R., Bandegi, A. R., & Miladi-gorji, H. (2017). Effects of prolonged abstinence from METH on the hippocampal BDNF levels, neuronal numbers and apoptosis in methamphetamine-sensitized rats. Neuroscience Letters, 645, 80-85. doi: http://dx.doi.org/10.1016/j.neulet.2017.02.051.

Krishnasamy, S., Weng, Y.-C., Thammisetty, S. S., Phaneuf, D., Lalancette-Hebert, M., & Kriz, J. (2017). Molecular imaging of nestin in neuroinflammatory conditions reveals marked signal induction in activated microglia. Journal of neuroinflammation, 14(1), 45. doi: 10.1186/s12974-017-0816-7.

Langley, M., Ghosh, A., Charli, A., Sarkar, S., Ay, M., Luo, J., . . . Kanthasamy, A. (2017). Mito-apocynin Prevents Mitochondrial Dysfunction, Microglial Activation, Oxidative Damage and Progressive Neurodegeneration in MitoPark Transgenic Mice. Antioxidants & redox signaling. doi: 10.1089/ars.2016.6905.

Leal-Campanario, R., Alarcon-Martinez, L., Rieiro, H., Martinez-Conde, S., Alarcon-Martinez, T., Zhao, X., . . . Macknik, S. L. (2017). Abnormal Capillary Vasodynamics Contribute to Ictal Neurodegeneration in Epilepsy.  Scientific Reports, 7, 43276. doi: 10.1038/srep43276

Mao, Z., Liu, C., Ji, S., Yang, Q., Ye, H., Han, H., & Xue, Z. (2017). The NLRP3 Inflammasome is Involved in the Pathogenesis of Parkinson’s Disease in Rats. Neurochemical Research, 1-12. doi: 10.1007/s11064-017-2185-0.

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Researchers cited MBF systems in 12 papers during the week of 02/27/2017

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Cao, M., Wu, Y., Ashrafi, G., McCartney, A. J., Wheeler, H., Bushong, E. A., . . . De Camilli, P. (2017). Parkinson Sac Domain Mutation in Synaptojanin 1 Impairs Clathrin Uncoating at Synapses and Triggers Dystrophic Changes in Dopaminergic Axons. Neuron, 93(4), 882-896.e885. doi: http://dx.doi.org/10.1016/j.neuron.2017.01.019.

Makinson, C. D., Tanaka, B. S., Sorokin, J. M., Wong, J. C., Christian, C. A., Goldin, A. L., . . . Huguenard, J. R. (2017). Regulation of Thalamic and Cortical Network Synchrony by Scn8a. Neuron. doi: http://dx.doi.org/10.1016/j.neuron.2017.01.031.

Mor, D. E. (2016). The toxic interaction of dopamine and alpha-synuclein: Implications for Parkinson’s disease. University of Pennsylvania. Retrieved from http://search.proquest.com/openview/28281453309e818989ee516dd6262df1/1?p….

Patzlaff, N. E., Nemec, K. M., Malone, S. G., Li, Y., & Zhao, X. (2017). Fragile X related protein 1 (FXR1P) regulates proliferation of adult neural stem cells. Human Molecular Genetics.

Shepherd, D. (2016). Examining the effects of anti-Nogo-A immunotherapy on post-stroke neurogenesis in the adult rat. Loyola University Chicago. Retrieved from http://search.proquest.com/openview/f196ea3a12bdd002c1a443d44292c2a4/1?p….

Shobin, E., Bowley, M. P., Estrada, L. I., Heyworth, N. C., Orczykowski, M. E., Eldridge, S. A., . . . Rosene, D. L. (2017). Microglia activation and phagocytosis: relationship with aging and cognitive impairment in the rhesus monkey. GeroScience, 1-22. doi: 10.1007/s11357-017-9965-y.

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Exercise changes astrocytes and eases symptoms of neurodegenerative disorders

Astrocytes (GFAP) in the dentate gyrus of a mouse hippocampus. Image courtesy of Dr. Ahmad Salehi, Stanford University. 

It is well known that physical exercise eases the symptoms of neurodegenerative disorders like Alzheimer’s disease and helps to prevent their onset. Researchers at Stanford University are working on figuring out how it happens.

In their study, published in the journal Brain Structure and Function, scientists in Dr. Ahmad Salehi’s lab examined the effects of physical exercise on astrocytes in a region of the mouse brain that is critical for cognition – the dentate gyrus of the hippocampus. Previous studies have shown that an increase in the expression of brain-derived neurotrophic factor (Bdnf) occurs in this region after exercise (Philips, Salehi et al 2014). Bdnf is a protein that supports the survival of existing neurons and encourages new growth, playing an important role in cognitive function.

While the current study reconfirms that exercise generates increased levels of Bdnf (more than a fourfold increase in exercised mice versus non-exercised mice), it also describes several new findings including increased synaptic load in the dentate gyrus, alterations in the morphology of astrocytes, and changes in the orientation of astrocytic projections toward dentate granule cells.

The authors speculate that the changes they observed may be attributed to increased expression of a receptor called TrkB, which astrocytes express in response to increases in Bdnf levels. According to the paper, TrkB binds to Bdnf, activating the mechanisms behind neuronal development.

“Our study suggests that astrocytes actively respond and could indeed mediate the positive effects of physical exercise on the central nervous system and potentially counter degenerative processes during aging and neurodegenerative disorders,” (Fahimi, et al 2016).

The researchers used Neurolucida to determine the location, the extent, and orientation of astrocytic projections, finding a significant increase in the length of astrocytic projections in exercised mice.

“Neurolucida is one of the very few systems that combines complex morphometrical quantification with beautiful display of the results,” said Dr. Salehi, Clinical Professor, Department of Psychiatry and Behavioral Sciences at Stanford Medical School.

Since astrocytes help prevent excitotoxicity in the brain by removing excess glutamate from extracellular space, the researchers speculate that the increased length of astrocytic projections they observed in exercised mice could make this process more efficient.

Differences in the orientation of astrocytic projections were also reported, with the majority of projections of exercised mice directed toward the dentate granule cell layer – a region featuring increased levels of Bdnf release and synthesis after exercise.

The number of astrocytes in the molecular layer of the dentate gyrus in exercised and non-exercised mice was quantified with Stereo Investigator, however, there was no significant difference in astrocyte populations between the two groups.

“In summary, our study suggests that astrocytes constitute an important element in mediating the positive effects of physical exercise in the dentate gyrus of the hippocampus. Furthermore, it appears that physical exercise-induced release of Bdnf by the DG leads to a significant alteration in structure and function of astrocytes in protection against glutamate toxicity during aging and a number of neurodegenerative disorders,” (Fahimi et al 2016)

Fahimi, A., Baktir, M.A., Moghadam, S., Mojabi, F.S., Sumanth, K., McNerney, M.W., Ponnusamy, R., Salehi, A. Brain Struct Funct (2016). doi:10.1007/s00429-016-1308-8

Phillips, C., Baktir, M.A., Srivatsam, M., Salehi, A. Front. Cell. Neurosci., (2014) https://doi.org/10.3389/fncel.2014.00170

Researchers cited MBF systems in 14 papers between 1/20/2017 and 1/27/2017

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Doerr, J., Schwarz, M. K., Wiedermann, D., Leinhaas, A., Jakobs, A., Schloen, F., . . . Brüstle, O. (2017). Whole-brain 3D mapping of human neural transplant innervation. Nature Communications, 8, 14162. doi: 10.1038/ncomms14162

Fields, J. A., Metcalf, J., Overk, C., Adame, A., Spencer, B., Wrasidlo, W., . . . Masliah, E. (2017). The anticancer drug sunitinib promotes autophagyand protects from neurotoxicity in an HIV-1 Tat model of neurodegeneration. Journal of Neurovirology, 1-14. doi: 10.1007/s13365-016-0502-z.

Haidar, M., Guèvremont, G., Zhang, C., Bathgate, R. A. D., Timofeeva, E., Smith, C. M., & Gundlach, A. L. (2017). Relaxin-3 Inputs Target Hippocampal Interneurons and Deletion of Hilar Relaxin-3 Receptors in ‘Floxed-RXFP3′ Mice Impairs Spatial Memory. Hippocampus, n/a-n/a. doi: 10.1002/hipo.22709.

Kelly, S. C., He, B., Perez, S. E., Ginsberg, S. D., Mufson, E. J., & Counts, S. E. (2017). Locus coeruleus cellular and molecular pathology during the progression of Alzheimer’s disease. Acta Neuropathologica Communications, 5(1), 8. doi: 10.1186/s40478-017-0411-2.

Shen, X.-L., Song, N., Du, X.-X., Li, Y., Xie, J.-X., & Jiang, H. (2017). Nesfatin-1 protects dopaminergic neurons against MPP+/MPTP-induced neurotoxicity through the C-Raf–ERK1/2-dependent anti-apoptotic pathway. Scientific Reports, 7, 40961. doi: 10.1038/srep40961

Turner, R. C., Naser, Z. J., Lucke-Wold, B. P., Logsdon, A. F., Vangilder, R. L., Matsumoto, R. R., . . . Rosen, C. L. (2017). Single low-dose lipopolysaccharide preconditioning: neuroprotective against axonal injury and modulates glial cells. [Lipopolysaccharide preconditioning, oncostatin M receptor, diffuse axonal injury, gliosis, neuroprotection]. Neuroimmunology and Neuroinflammation, 4(1), 6-15.

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