New Software Released for Automated Neuron Reconstruction and Analysis

montage for email invitationHow the brain works and how the brain is affected by disease are mysteries in large part because neurons are so dynamic, numerous, and complex. Neurolucida 360, a revolutionary, new software product from MBF Bioscience, enables neuroscientists to uncover more information about neurons at a faster rate.

“Neurolucida 360 is a technological revolution” says Jack Glaser, President of MBF Bioscience. “It is the state-of-the-art tool for neuroscientists to analyze the shape and connectivity of neurons more quickly and accurately than has ever been possible, so that we can better understand the brain and the mechanisms behind diseases such as Alzheimer’s and Parkinson’s. With the unique ability to automatically detect and analyze dendrites, dendritic spines, axons, somas, and synapses, Neurolucida 360 is now the standardized platform for the global neuroscience research community to perform unprecedented investigations into the functioning of the brain.”

Using automated tools in Neurolucida 360, researchers generate high-resolution, digital 3D reconstructions of neurons imaged with numerous microscopy techniques, including light sheet, 2 photon, confocal and brightfield. Using the most advanced algorithms for neuron reconstruction, researchers instantly receive hundreds of analyses about the size, shape, and complexity of neurons. The reliable data from Neurolucida 360 is integral to learning how injury, disease, or chemicals change neuronal structure, discovering how neuronal structure affects function, finding out which brain regions neurons communicate with, and more.

The National Institute of Mental Health provides funding to support the development Neurolucida 360. It is the latest development in the renowned legacy of neuron tracing tools that started with Neurolucida – the most widely cited tool for neuron reconstruction and analysis.

For more information on Neurolucida 360, please visit our website or watch this short video.

Researchers cited MBF systems in 22 papers between 11/13/2015 and 11/30/2015

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Divito, C. B., Steece-Collier, K., Case, D. T., Williams, S.-P. G., Stancati, J. A., Zhi, L., . . . Sulzer, D. (2015). Loss of VGLUT3 Produces Circadian-Dependent Hyperdopaminergia and Ameliorates Motor Dysfunction and l-Dopa-Mediated Dyskinesias in a Model of Parkinson’s Disease. The Journal of Neuroscience, 35(45), 14983-14999.

English, S. J., Diaz, J. A., Shao, X., Gordon, D., Bevard, M., Su, G., . . . Piert, M. (2014). Utility of 18 F-FDG and 11C-PBR28 microPET for the assessment of rat aortic aneurysm inflammation. EJNMMI Research, 4(1), 1-29.

Giovanoli, S., Notter, T., Richetto, J., Labouesse, M., Vuillermot, S., Riva, M., & Meyer, U. (2015). Late prenatal immune activation causes hippocampal deficits in the absence of persistent inflammation across aging. Journal of neuroinflammation, 12(1), 221.

Jacky, W. (2015). Neuropathologic features in the hippocampus and cerebellum of three older men with fragile X syndrome.

Jenkins, B., Zhu, A., Poutiainen, P., Choi, J.-K., Kil, K.-E., Zhang, Z., . . . Brownell, A.-L. (2015). Functional modulation of G-protein coupled receptors during Parkinson disease-like neurodegeneration. Neuropharmacology. doi:

Lee, Y.-I., Kang, H., Ha, Y. W., Chang, K.-Y., Cho, S.-C., Song, S. O., . . . Shin, J.-H. (2015). Diaminodiphenyl sulfone-induced parkin ameliorates age-dependent dopaminergic neuronal loss. Neurobiology of Aging. doi:

Mauney, S. A., Pietersen, C. Y., Sonntag, K.-C., & Woo, T.-U. W. (2015). Differentiation of oligodendrocyte precursors is impaired in the prefrontal cortex in schizophrenia. Schizophrenia Research. doi:

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Researchers cited MBF systems in 24 papers between 11/2/2015 and 11/13/2015

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Bains, M., & Roberts, J. L. (2015). Estrogen protects against dopamine neuron toxicity in primary mesencephalic cultures through an indirect P13K/Akt mediated astrocyte pathway. Neuroscience Letters. doi:

Chen, M.-h., Liu, Y.-h., Xu, H., Xu, D.-w., Wang, C.-n., Wang, Y., . . . Wang, Y.-h. (2015). Lentiviral Vector-Mediated p27kip1 Expression Facilitates Recovery After Spinal Cord Injury. Molecular Neurobiology, 1-14. doi: 10.1007/s12035-015-9498-2.

Correa, M., Pardo, M., Bayarri, P., López-Cruz, L., San Miguel, N., Valverde, O., . . . Salamone, J. (2015). Choosing voluntary exercise over sucrose consumption depends upon dopamine transmission: effects of haloperidol in wild type and adenosine A2AKO mice. Psychopharmacology, 1-12. doi: 10.1007/s00213-015-4127-3.

Fragale, J. E. C., Khariv, V., Gregor, D. M., Smith, I. M., Jiao, X., Elkabes, S., . . . Beck, K. D. (2016). Dysfunction in amygdala–prefrontal plasticity and extinction-resistant avoidance: A model for anxiety disorder vulnerability. Experimental Neurology, 275, Part 3, 59-68. doi:

Goodus, M. T., Kerr, N. A., Talwar, R., Buziashvili, D., Fragale, J. E. C., Pang, K., & Levison, S. W. (2015). LIF Haplodeficiency Desynchronizes Glial Reactivity and Exacerbates Damage and Functional Deficits After a Concussive Brain Injury. Journal of Neurotrauma. doi: 10.1089/neu.2015.4234.

Huang, Q., Du, X., He, X., Yu, Q., Hu, K., Breitwieser, W., . . . Li, M. (2015). JNK-mediated activation of ATF2 contributes to dopaminergic neurodegeneration in the MPTP mouse model of Parkinson’s disease. Experimental Neurology. doi:

Jayasinghe, V. R., Flores-Barrera, E., West, A. R., & Tseng, K. Y. (2015). Frequency-Dependent Corticostriatal Disinhibition Resulting from Chronic Dopamine Depletion: Role of Local Striatal cGMP and GABA-AR Signaling. Cerebral Cortex. doi: 10.1093/cercor/bhv241.

Kohl, Z., Abdallah, N. B., Vogelgsang, J., Tischer, L., Deusser, J., Amato, D., . . . Winkler, J. (2015). Severely impaired hippocampal neurogenesis associates with an early serotonergic deficit in a BAC α-synuclein transgenic rat model of Parkinson’s disease. Neurobiology of Disease. doi:

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Dying neurons in Alzheimer’s patients show signs of improvement after gene therapy

nucleus basalis of Meynert

Micrograph of cholinergic neurons in the nucleus basalis of Meynert. Image from Wikipedia.


Cholinergic neurons degenerate at devastating rates in Alzheimer’s disease, but Dr. Mark Tuszynski and his team at the University of California, San Diego may have found a way to slow the decline.

Their study, published in JAMA Neurology, reports that nerve growth factor gene therapy increased the size, axonal sprouting, and signaling of cholinergic neurons in 10 Alzheimer’s disease patients.

The patients were enrolled in a clinical trial between 2001 and 2012. Ex vivo and in vivo methods of gene therapy were used to deliver nerve growth factor – a protein that protects neurons and stimulates growth – to the patients. Eight received an implant of their own skin cells that were genetically modified to express nerve growth factor (ex vivo ) and two patients received injections that induced neurons already in the brain to express nerve growth factor (in vivo). In all 10 patients, gene therapy was delivered to the nucleus basalis of Meynert – part of the basal forebrain rich in cholinergic neurons that undergoes degeneration during Alzheimer’s disease. 

The patients’ survival time ranged from one to 10 years. After they had died, researchers analyzed the effects of nerve growth factor on cholinergic neurons.

The axons of cholinergic neurons, labeled with p75, grew toward the source of the nerve growth factor in all 10 patients. To determine if there was a change in cell size, researchers used the nucleator probe in Stereo Investigator to analyze cholinergic neurons of 3 patients who received gene therapy via the ex vivo method in one hemisphere – the other hemisphere was used as a control. Results from Stereo Investigator showed that cell bodies were larger in the treated hemisphere vs. the untreated hemisphere.

Finally, to find out if nerve growth factor induced signaling within cells, the researchers analyzed the amount of CREB and c-fos – markers for cell activation – in 2 patients who received nerve growth factor in vivo. An elevated amount of CREB and c-fos was found when compared to control regions. Neurons exhibiting tau pathology also expressed nerve growth factor, indicating that degenerating cells could respond to nerve growth factor gene therapy.

A phase 2 clinical study is currently under way to report cognitive outcomes in patients with Alzheimer’s disease.

“Collectively, these anatomical findings support the rationale for clinical trials to test the hypothesis that sustained growth factor delivery over time can reduce cell degeneration and stimulate cell function in chronic neurodegenerative disorders, thereby slowing functional decline,” Tuszynski, et al.

Tuszynski, M.H., Yang, J.H., Pay, M.M., Masliah, E., Barba, D., U, H.S., Conner, J.M., Kobalka, P., Roy, S., and Nagahara A.H. (2015). Nerve Growth Factor Gene Therapy: Activation of Neuronal Responses in Alzheimer Disease. JAMA Neurology, published online August 24, 2015. DOI: 10.1001/jamaneurol.2015.1807.

Researchers cited MBF systems in 19 papers during the week of 10/26/2015

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Bernstock, J. D., Lee, Y.-j., Peruzzotti-Jametti, L., Southall, N., Johnson, K. R., Maric, D., . . . Hallenbeck, J. M. (2015). A novel quantitative high-throughput screen identifies drugs that both activate SUMO conjugation via the inhibition of microRNAs 182 and 183 and facilitate neuroprotection in a model of oxygen and glucose deprivation. Journal of Cerebral Blood Flow and Metabolism. doi: 10.1177/0271678×15609939.

Haeussner, E., Aschauer, B., Burton, G. J., Huppertz, B., Edler von Koch, F., Müller-Starck, J., . . . Frank, H.-G. (2015). Does 2D-Histologic identification of villous types of human placentas at birth enable sensitive and reliable interpretation of 3D structure? Placenta. doi:

Kumar, A., Alvarez-Croda, D.-M., Stoica, B. A., Faden, A. I., & Loane, D. J. (2015). Microglial/macrophage polarization dynamics following traumatic brain injury. Journal of Neurotrauma. doi: 10.1089/neu.2015.4268.

Nam, J. H., Park, E. S., Won, S.-Y., Lee, Y. A., Kim, K. I., Jeong, J. Y., . . . Jin, B. K. (2015). TRPV1 on astrocytes rescues nigral dopamine neurons in Parkinson’s disease via CNTF. [10.1093/brain/awv297]. Brain.

Peck, J. D., Quaas, A. M., Craig, L. B., Soules, M. R., Klein, N. A., & Hansen, K. R. (2015). Lifestyle factors associated with histologically derived human ovarian non-growing follicle count in reproductive age women. Human Reproduction. doi: 10.1093/humrep/dev271.

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Researchers cited MBF systems in 15 papers during the week of 10/19/2015

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Bingol, F., Yoruk, O., Bingol, B. O., Erdemci, B., Ozkan, O., & Mazlumoglu, M. R. (2015). Estimation of the efficacy of chemo-radiotherapy on tumor regression in the patients with laryngeal cancer via computerized tomography using the Cavalieri method. Acta Oto-Laryngologica, 1-4. doi: 10.3109/00016489.2015.1096958.

Darlot, F., Moro, C., El Massri, N., Chabrol, C., Johnstone, D. M., Reinhart, F., . . . Benabid, A.-L. (2015). Near-infrared light is neuroprotective in a monkey model of Parkinson’s disease. Annals of Neurology, n/a-n/a. doi: 10.1002/ana.24542.

McConnell, E. D., Wei, H. S., Reitz, K. M., Kang, H., Takano, T., Vates, G. E., & Nedergaard, M. (2015). Cerebral microcirculatory failure after subarachnoid hemorrhage is reversed by hyaluronidase. Journal of Cerebral Blood Flow and Metabolism. doi: 10.1177/0271678×15608389.

Prokop, S., Miller, K. R., Drost, N., Handrick, S., Mathur, V., Luo, J., . . . Heppner, F. L. (2015). Impact of peripheral myeloid cells on amyloid-β pathology in Alzheimer’s disease–like mice. The Journal of Experimental Medicine, 212(11), 1811-1818. doi: 10.1084/jem.20150479.

Rocha, M. C., Grady, J. P., Grünewald, A., Vincent, A., Dobson, P. F., Taylor, R. W., . . . Rygiel, K. A. (2015). A novel immunofluorescent assay to investigate oxidative phosphorylation deficiency in mitochondrial myopathy: understanding mechanisms and improving diagnosis. Scientific Reports, 5, 15037. doi: 10.1038/srep15037

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Researchers cited MBF systems in 17 papers during the week of 10/12/2015

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Bollinger, J. L., Bergeon Burns, C. M., & Wellman, C. L. (2015). Differential Effects of Stress on Microglial Cell Activation in Male and Female Medial Prefrontal Cortex. Brain, Behavior, and Immunity. doi:

Brace, L. R., Kraev, I., Rostron, C. L., Stewart, M. G., Overton, P. G., & Dommett, E. J. (2015). Auditory responses in a rodent model of Attention Deficit Hyperactivity Disorder. Brain Research. doi:

Engin, E., Zarnowska, E. D., Benke, D., Tsvetkov, E., Sigal, M., Keist, R., . . . Rudolph, U. (2015). Tonic Inhibitory Control of Dentate Gyrus Granule Cells by α5-Containing GABAA Receptors Reduces Memory Interference. The Journal of Neuroscience, 35(40), 13698-13712.

Maia, G. H., Soares, J. I., Andrade, P. A., Leite, J. F., Luz, L. L., Andrade, J. P., & Lukoyanov, N. V. (2015). Altered taste preference and loss of limbic-projecting serotonergic neurons in the dorsal raphe nucleus of chronically epileptic rats. Behavioural Brain Research. doi:

Markram, H., Muller, E., Ramaswamy, S., Reimann, Michael W., Abdellah, M., Sanchez, Carlos A., . . . Schürmann, F. (2015). Reconstruction and Simulation of Neocortical Microcircuitry. Cell, 163(2), 456-492. doi:

Pagliarini, V., Pelosi, L., Bustamante, M. B., Nobili, A., Berardinelli, M. G., D’Amelio, M., . . . Sette, C. (2015). SAM68 is a physiological regulator of SMN2 splicing in spinal muscular atrophy. The Journal of Cell Biology, 211(1), 77-90. doi: 10.1083/jcb.201502059.

Salaj, M., Druga, R., Cerman, J., Kubová, H., & Barinka, F. (2015). Calretinin and parvalbumin immunoreactive interneurons in the retrosplenial cortex of the rat brain: Qualitative and quantitative analyses. Brain Research. doi:

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Researchers cited MBF systems in 22 papers during the week of 10/5/2015

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Abeysinghe, H. S., Bokhari, L., Quigley, A., Choolani, M., Chan, J., Dusting, G., . . . Roulston, C. (2015). Pre-differentiation of human neural stem cells into GABAergic neurons prior to transplant results in greater repopulation of the damaged brain and accelerates functional recovery after transient ischemic stroke. Stem Cell Research & Therapy, 6(1), 1-19. doi: 10.1186/s13287-015-0175-1.

Alter, S. P., Stout, K. A., Lohr, K. M., Taylor, T. N., Shepherd, K. R., Wang, M., . . . Miller, G. W. (2015). Reduced vesicular monoamine transport disrupts serotonin signaling but does not cause serotonergic degeneration. Experimental Neurology. doi:

Brock, J. H., Graham, L., Staufenberg, E., Collyer, E., Koffler, Y., & Tuszynski, M. H. (2015). Bone Marrow Stromal Cell Intraspinal Transplants Fail to Improve Motor Outcomes in a Severe Model of Spinal Cord Injury. Journal of Neurotrauma. doi: 10.1089/neu.2015.4009.

Büchele, F., Morawska, M. M., Schreglmann, S. R., Penner, M., Muser, M., Baumann, C. R., & Noain, D. (2015). Novel rat model of weight drop-induced closed diffuse traumatic brain injury compatible with electrophysiological recordings of vigilance states. Journal of Neurotrauma. doi: 10.1089/neu.2015.4001.

Fukusumi, Y., Meier, F., Götz, S., Matheus, F., Irmler, M., Beckervordersandforth, R., . . . Zhang, J. (2015). Dickkopf 3 Promotes the Differentiation of a Rostrolateral Midbrain Dopaminergic Neuronal Subset In Vivo and from Pluripotent Stem Cells In Vitro in the Mouse. The Journal of Neuroscience, 35(39), 13385-13401

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Researchers cited MBF systems in 16 papers during the week of 9/28/2015

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Giovanoli, S., Weber-Stadlbauer, U., Schedlowski, M., Meyer, U., & Engler, H. (2015). Prenatal immune activation causes hippocampal synaptic deficits in the absence of overt microglia anomalies. Brain, Behavior, and Immunity. doi:

Gokozan, H. N., Baig, F., Corcoran, S., Catacutan, F. P., Gygli, P. E., Takakura, A. C., . . . Otero, J. J. (2015). Area postrema undergoes dynamic postnatal changes in mice and humans. Journal of Comparative Neurology, n/a-n/a. doi: 10.1002/cne.23903.

Huebner, S. M., Tran, T. D., Rufer, E. S., Crump, P. M., & Smith, S. M. (2015). Maternal Iron Deficiency Worsens the Associative Learning Deficits and Hippocampal and Cerebellar Losses in a Rat Model of Fetal Alcohol Spectrum Disorders. Alcoholism: Clinical and Experimental Research, n/a-n/a. doi: 10.1111/acer.12876.

Maiti, P., Gregg, L. C., & McDonald, M. P. (2015). MPTP-induced executive dysfunction is associated with altered prefrontal serotonergic function. Behavioural Brain Research. doi:

Odacı, E., Hancı, H., İkinci, A., Sönmez, O. F., Aslan, A., Şahin, A., . . . Baş, O. (2015). Maternal exposure to a continuous 900-MHz electromagnetic field provokes neuronal loss and pathological changes in cerebellum of 32-day-old female rat offspring. Journal of Chemical Neuroanatomy. doi:

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Researchers cited MBF systems in 14 papers between 9/11/2015 and 9/25/2015

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Beraldi, R., Chan, C.-H., Rogers, C. S., Kovács, A. D., Meyerholz, D. K., Trantzas, C., . . . Pearce, D. A. (2015). A novel porcine model of Ataxia Telangiectasia reproduces neurological features and motor deficits of human disease. Human Molecular Genetics. doi: 10.1093/hmg/ddv356.

Bernardes, D., Brambilla, R., Bracchi-Ricard, V., Karmally, S., Dellarole, A., Carvalho-Tavares, J., & Bethea, J. R. (2015). Prior regular exercise improves clinical outcome and reduces demyelination and axonal injury in experimental autoimmune encephalomyelitis. Journal of Neurochemistry, n/a-n/a. doi: 10.1111/jnc.13354.

Montalvo-Javé, E. E., Mendoza-Barrera, G. E., García-Pineda, M. A., Jaime Limón, Á. R., Montalvo-Arenas, C., Castell Rodríguez, A. E., & Tapia Jurado, J. (2015). Histological Analysis of Intra-Abdominal Adhesions Treated with Sodium Hyaluronate and Carboxymethylcellulose Gel. Journal of Investigative Surgery, 1-8. doi: 10.3109/08941939.2015.1076911.

Ruiz, M., Perez-Garcia, G., Ortiz-Virumbrales, M., Méneret, A., Morant, A., Kottwitz, J., . . . Ehrlich, M. E. (2015). Abnormalities of motor function, transcription and cerebellar structure in mouse models of THAP1 dystonia. Human Molecular Genetics. doi: 10.1093/hmg/ddv384.

Weisheit, C. E., & Dauer, W. T. (2015). A novel conditional knock-in approach defines molecular and circuit effects of the DYT1 dystonia mutation. Human Molecular Genetics. doi: 10.1093/hmg/ddv355.


Ahn, S., Kim, T.-G., Kim, K.-S., & Chung, S. (2015). Differentiation of human pluripotent stem cells into medial ganglionic eminence vs. caudal ganglionic eminence cells. Methods.

Hsieh, J. T., Lei, B., Sheng, H., Venkatraman, T., Lascola, C. D., Warner, D. S., & James, M. L. (2015). Sex-Specific Effects of Progesterone on Early Outcome of Intracerebral Hemorrhage. Neuroendocrinology.

Jiang, Y., Pun, R. Y. K., Peariso, K., Holland, K. D., Lian, Q., & Danzer, S. C. (2015). Olfactory Bulbectomy Leads to the Development of Epilepsy in Mice. Plos one, 10(9), e0138178. doi: 10.1371/journal.pone.0138178.

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