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

Stereo Investigator:journal images sm

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.

Continue reading “Researchers cited MBF systems in 27 papers between 3/20/2017 and 3/30/2017” »

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

Stereo Investigator:journal images sm

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.

Continue reading “Researchers cited MBF systems in 28 papers during the week of 03/06/2017” »

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

Stereo Investigator:journal images sm

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.

Continue reading “Researchers cited MBF systems in 12 papers during the week of 02/27/2017” »

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

Stereo Investigator: journal images sm

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.

Continue reading “Researchers cited MBF systems in 14 papers between 1/20/2017 and 1/27/2017” »

Researchers cited MBF systems in 25 papers between 1/13/2017 and 1/20/2017

Stereo Investigator:journal images sm

Allegra, M., Spalletti, C., Vignoli, B., Azzimondi, S., Busti, I., Billuart, P., . . . Caleo, M. (2017). Pharmacological rescue of adult hippocampal neurogenesis in a mouse model of X-linked intellectual disability. Neurobiology of Disease, 100, 75-86.

Anan, J., Hijioka, M., Kurauchi, Y., Hisatsune, A., Seki, T., & Katsuki, H. (2017). Cortical hemorrhage-associated neurological deficits and tissue damage in mice are ameliorated by therapeutic treatment with nicotine. Journal of Neuroscience Research, n/a-n/a. doi: 10.1002/jnr.24016.

Ardestani, P. M., Evans, A. K., Yi, B., Nguyen, T., Coutellier, L., & Shamloo, M. (2017). Modulation of neuroinflammation and pathology in the 5XFAD mouse model of Alzheimer’s disease using a biased and selective beta-1 adrenergic receptor partial agonist. Neuropharmacology.

Estrada, L. I., Robinson, A. A., Amaral, A. C., Giannaris, E. L., Heyworth, N. C., Mortazavi, F., . . . Rosene, D. L. (2017). Evaluation of Long-Term Cryostorage of Brain Tissue Sections for Quantitative Histochemistry. Journal of Histochemistry and Cytochemistry, 0022155416686934. doi: 10.1369/0022155416686934.

Klocke, C., Allen, J. L., Sobolewski, M., Mayer-Pröschel, M., Blum, J. L., Lauterstein, D., . . . Cory-Slechta, D. A. (2017). Neuropathological Consequences of Gestational Exposure to Concentrated Ambient Fine and Ultrafine Particles in the Mouse. Toxicological Sciences. doi: 10.1093/toxsci/kfx010.

Loris, Z. B., Pieper, A. A., & Dalton Dietrich, W. (2017). The neuroprotective compound P7C3-A20 promotes neurogenesis and improves cognitive function after ischemic stroke. Experimental Neurology, 290, 63-73. doi: http://dx.doi.org/10.1016/j.expneurol.2017.01.006.

Luo, L., Chen, J., Su, D., Chen, M., Luo, B., Pi, R., . . . Wang, R. (2017). L-F001, a Multifunction ROCK Inhibitor Prevents 6-OHDA Induced Cell Death Through Activating Akt/GSK-3beta and Nrf2/HO-1 Signaling Pathway in PC12 Cells and Attenuates MPTP-Induced Dopamine Neuron Toxicity in Mice. Neurochemical Research, 1-10. doi: 10.1007/s11064-016-2117-4.

Moore, B. A., Tyrrell, L. P., Pita, D., Bininda-Emonds, O. R. P., & Fernández-Juricic, E. (2017). Does retinal configuration make the head and eyes of foveate birds move? . Scientific Reports, 7, 38406. doi: 10.1038/srep38406

Continue reading “Researchers cited MBF systems in 25 papers between 1/13/2017 and 1/20/2017” »

Uncovering the role of microglia in fetal alcohol spectrum disorders

microglia_alcohol

Representative images of Iba-1+ microglia in the postnatal day 10 rat hippocampus. Image courtesy of Anna Klintsova, PhD.

Children born with fetal alcohol spectrum disorders face a range of physical and cognitive impairments including long-term deficits in learning, behavior, and immune function. In a paper published in Neuroscience, Dr. Anna Klintsova and her lab at the University of Delaware report that activation of the brain’s immune response may contribute to some of the damage caused by fetal alcohol spectrum disorders.

In their study, the researchers used Stereo Investigator and Neurolucida to examine the hypothesis that exposure to alcohol while the brain is growing rapidly is associated with abnormal microglial activation and high levels of pro-inflammatory proteins which impair learning-related plasticity; leading to neuro-developmental and psychopathological disorders.

“My lab has been using both Stereo Investigator and Neurolucida for more than a decade in all quantitative neuroanatomical studies, including the featured one,” said Dr. Anna Klintsova. “We find this software to be user-friendly, reliable and essential for obtaining unbiased results.”

They used Stereo Investigator to quantify the number of microglia in the hippocampus of neonatal rats who were exposed to alcohol during the equivalent of the third trimester of a human pregnancy. The researchers expected to see an increased number of microglia in alcohol-exposed neonatal rats, however they found a decreased number of microglia. Despite the decrease in microglia number, there was a significant increase in pro-inflammatory proteins expressed by microglia and an increase in microglial activation.

To measure microglial activation, the researchers quantified the area of cell territory using Neurolucida. Activated microglia have a smaller cell territory than resting microglia, so the smaller cell territory found in alcohol exposed rats indicates a more active state.

This research supports the hypothesis that abnormal microglia activation plays a role in fetal alcohol spectrum disorders, however more research is needed to further understand the relationship.

Boschen, K., Ruggiero, M.J., Klintsova, A.Y., (2016) Neonatal binge alcohol exposure increases microglial activation in the developing rat hippocampus. Neuroscience 324: 355–366. DOI: 10.1016/j.neuroscience.2016.03.033

 

Researchers cited MBF systems in 21 papers between 12/16/2016 and 1/6/2017

Stereo Investigator:journal images sm

Campolo, M., Casili, G., Biundo, F., Crupi, R., Cordaro, M., Cuzzocrea, S., & esposito, e. (2016). The neuroprotective effect of dimethyl fumarate in a MPTP-mouse model of Parkinson’s disease: involvement of reactive oxygen species/nuclear factor-κB/nuclear transcription factor related to NF-E2. Antioxidants & redox signaling. doi: 10.1089/ars.2016.6800.

Charvet, C. J., Stimpson, C. D., Kim, Y. D., Raghanti, M. A., Lewandowski, A. H., Hof, P. R., . . . Sherwood, C. C. (2016). Gradients in cytoarchitectural landscapes of the isocortex: diprotodont marsupials in comparison to eutherian mammals. Journal of Comparative Neurology, n/a-n/a. doi: 10.1002/cne.24160.

Embury, C. M., Dyavarshetty, B., Lu, Y., Wiederin, J. L., Ciborowski, P., Gendelman, H. E., & Kiyota, T. (2016). Cathepsin B Improves ß-Amyloidosis and Learning and Memory in Models of Alzheimer’s Disease. Journal of Neuroimmune Pharmacology, 1-13. doi: 10.1007/s11481-016-9721-6.

Güleç, A., Bakkalbaşı, B. Ç., Cumbul, A., Uslu, Ü., Alev, B., & Yarat, A. (2017). Effects of local platelet-rich plasma injection on the rate of orthodontic tooth movement in a rat model: A histomorphometric study. American Journal of Orthodontics and Dentofacial Orthopedics, 151(1), 92-104. doi: http://dx.doi.org/10.1016/j.ajodo.2016.05.016.

Hoeijmakers, L., Ruigrok, S. R., Amelianchik, A., Ivan, D., Dam, A.-M. v., Lucassen, P. J., & Korosi, A. (2017). Early-life stress lastingly alters the neuroinflammatory response to amyloid pathology in an Alzheimer’s disease mouse model. Brain, Behavior, and Immunity. doi: http://dx.doi.org/10.1016/j.bbi.2016.12.023.

Continue reading “Researchers cited MBF systems in 21 papers between 12/16/2016 and 1/6/2017” »

Researchers cited MBF systems in 18 papers during the week of 12/12/2016

Stereo Investigator:journal images sm

Alberico, S. L., Kim, Y.-C., Lence, T., & Narayanan, N. S. (2016). Axial levodopa-induced dyskinesias and neuronal activity in the dorsal striatum. Neuroscience. doi: http://dx.doi.org/10.1016/j.neuroscience.2016.11.046.

Forgione, N., Chamankhah, M., & Fehlings, M. (2016). A Mouse Model of Bilateral Cervical Contusion-Compression Spinal Cord Injury. Journal of Neurotrauma. doi: 10.1089/neu.2016.4708.

Gasser, E., Johannssen, H. C., Rülicke, T., Zeilhofer, H. U., & Stoffel, M. (2016). Foxa1 is essential for development and functional integrity of the subthalamic nucleus. Scientific Reports, 6, 38611. doi: 10.1038/srep38611

Ghosh, A., Tyson, T., George, S., Hildebrandt, E. N., Steiner, J. A., Madaj, Z., . . . Brundin, P. (2016). Mitochondrial pyruvate carrier regulates autophagy, inflammation, and neurodegeneration in experimental models of Parkinson’s disease. [10.1126/scitranslmed.aag2210]. Science translational medicine, 8(368), 368ra174.

Jacinto, L. R., Mata, R., Novais, A., Marques, F., & Sousa, N. (2016). The habenula as a critical node in chronic stress-related anxiety. Experimental Neurology. doi: http://dx.doi.org/10.1016/j.expneurol.2016.12.003.

Jobe, E. M., Gao, Y., Eisinger, B. E., Mladucky, J. K., Giuliani, C. C., Kelnhofer, L. E., & Zhao, X. (2016). Methyl-CpG binding protein MBD1 regulates neuronal lineage commitment through maintaining adult neural stem cell identity. [10.1523/JNEUROSCI.1075-16.2016]. The Journal of Neuroscience.

Mandolesi, G., De Vito, F., Musella, A., Gentile, A., Bullitta, S., Fresegna, D., . . . Mori, F. (2016). miR-142-3p is a key regulator of IL-1β-dependent synaptopathy in neuroinflammation. Journal of Neuroscience, 0851-0816.

Continue reading “Researchers cited MBF systems in 18 papers during the week of 12/12/2016” »