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Journal articles on the topic 'Microencephaly'

Author: Grafiati

Published: 25 June 2021

Last updated: 17 February 2022

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1

Balduini, Walter, Lucio G. Costa, and Flaminio Cattabeni. "Molecular mechanisms involved in experimental microencephaly." Pharmacological Research 22 (September 1990): 26. http://dx.doi.org/10.1016/s1043-6618(09)80082-0.

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2

Garbossa, Diego, and Alessandro Vercelli. "Experimentally-induced microencephaly: effects on cortical neurons." Brain Research Bulletin 60, no. 4 (May 2003): 329–38. http://dx.doi.org/10.1016/s0361-9230(03)00053-4.

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3

Furukawa, Satoshi, Koji Usuda, Masayoshi Abe, Seigo Hayashi, and Izumi Ogawa. "Indole-3-acetic acid induces microencephaly in mouse fetuses." Experimental and Toxicologic Pathology 59, no. 1 (September 2007): 43–52. http://dx.doi.org/10.1016/j.etp.2006.12.001.

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4

Furukawa, Satoshi, Masayoshi Abe, Koji Usuda, and Izumi Ogawa. "Indole-3-Acetic Acid Induces Microencephaly in Rat Fetuses." Toxicologic Pathology 32, no. 6 (October 2004): 659–67. http://dx.doi.org/10.1080/01926230490520269.

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5

Shapira Zaltsberg, G., H. McMillan, and E. Miller. "P.067 Phosphoserine aminotransferase (PSAT) deficiency: Imaging findings in a child with congenital microcephaly." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 45, s2 (June 2018): S33. http://dx.doi.org/10.1017/cjn.2018.169.

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Background: Serine deficiency disorders can result from deficiency in one of three enzymes. Deficiency of the second enzyme in the serine biosynthesis pathway, 3-phosphoserine aminotransferase (PSAT), has been reported in two siblings when the eldest was investigated for acquired microcephaly, progressive spasticity and intractable epilepsy. Methods: Our patient had neurological symptoms apparent at birth. Fetal magnetic resonance imaging (MRI) at 35 weeks gestation demonstrated microencephaly and simplification of the the gyration (anterior>posterior) which was confirmed upon subsequent post-natal MRI. Congenital microcephaly was apparent at birth. Results: PSAT deficiency was confirmed when exome sequencing identified biallelic mutations in PSAT1; c.44C>T, p.Ala15Val and; c.432delA, p.Pro144fs and biochemical testing noted low plasma serine 22 mcmol/L (normal 83-212 mcmol/L) and low CSF serine 10 mcmol/L (normal 22-61 mcmol/L). Despite oral serine and glycine supplementation at 4 months old the patient showed little neurodevelopmental progress and developed epileptic spasms at 10 months old. Serological testing for TORCH infections was negative. Conclusions: PSAT deficiency should be considered for patients with congenital microcephaly. Although further characterization of MRI findings in other patients is required, microencephaly with simplified gyral pattern could provide imaging clues for this rare metabolic disorder.

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6

Cattabeni, F., M. P. Abbracchio, M. Cimino, D. Cocchi, M. Di Luca, L. Mennuni, F. Rosi, and P. Zaratin. "Methylazoxymethanol-induced microencephaly: persistent increase of cortical somatostatin-like immunoreactivity." Developmental Brain Research 47, no. 1 (May 1989): 156–59. http://dx.doi.org/10.1016/0165-3806(89)90120-x.

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7

Wichgers Schreur, P. J., L. van Keulen, D. Anjema, J. Kant, and J. Kortekaas. "Microencephaly in fetal piglets following in utero inoculation of Zika virus." Emerging Microbes & Infections 7, no. 1 (March 29, 2018): 1–11. http://dx.doi.org/10.1038/s41426-018-0044-y.

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8

Chandra, P. S., N. Salamon, S. T. Nguyen, J. W. Chang, M. N. Huynh, C. Cepeda, J. P. Leite, et al. "Infantile spasm-associated microencephaly in tuberous sclerosis complex and cortical dysplasia." Neurology 68, no. 6 (February 5, 2007): 438–45. http://dx.doi.org/10.1212/01.wnl.0000252952.62543.20.

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9

Naus, C. C. G., M. Cimino, G. R. Wood, M. Di Luca, and F. Cattabeni. "Cellular expression of somatostatin in MAM-induced microencephaly in the rat." Developmental Brain Research 70, no. 1 (November 1992): 39–46. http://dx.doi.org/10.1016/0165-3806(92)90101-2.

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10

Tamaru, Masao, Yukio Yoneda, Kiyokazu Ogita, Jun Shimizu, Tenhoshimaru Matsutani, and Yutaka Nagata. "Excitatory amino acid receptors in brains of rats with methylazoxymethanol-induced microencephaly." Neuroscience Research 14, no. 1 (June 1992): 13–25. http://dx.doi.org/10.1016/s0168-0102(05)80003-3.

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11

Kadek, Kadek, and S. Darmadi. "Congenital Rubella Syndrome Based on Serologic and RNA Virus Examination." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 13, no. 2 (February 22, 2017): 63. http://dx.doi.org/10.24293/ijcpml.v13i2.673.

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Rubella infection with occurs during pregnancy, especially during the first trimester often caused by Congenital Rubella Syndrome (CRS). CRS can resulting abortions, miscarriages, stillbirth, and severe birth defects. The baby diagnosed with CRS when characterized by signs or symptoms from the following two categories A (Cataracts/congenital glaucoma, congenital heart disease (most commonly patent ductus arteriosus or peripheral pulmonary artery stenosis), loss of hearing, pigmentary retinopathy) or one categorie A and one catagorie B (Purpura, splenomegaly, jaundice, microencephaly, mental retardation, meningoencephalitis, radiolucent bone disease. Laboratory confirmation can be obtained by any of the following: virus isolation, serologi test (pasif hemaglutination, latex agglutination test, hemaglutination inhibisi, Flouresence immunoassay, Enzyme immunoassay), RNA test.

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12

Kadek, Kadek, and S. Darmadi. "GEJALA RUBELA BAWAAN (KONGENITAL) BERDASARKAN PEMERIKSAAN SEROLOGIS DAN RNA VIRUS." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 13, no. 2 (March 15, 2018): 63. http://dx.doi.org/10.24293/ijcpml.v13i2.885.

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Rubella infection with occurs during pregnancy, especially during the first trimester often caused by Congenital Rubella Syndrome(CRS). CRS can resulting abortions, miscarriages, stillbirth, and severe birth defects. The baby diagnosed with CRS when characterizedby signs or symptoms from the following two categories A (Cataracts/congenital glaucoma, congenital heart disease (most commonlypatent ductus arteriosus or peripheral pulmonary artery stenosis), loss of hearing, pigmentary retinopathy) or one categorie A andone catagorie B (Purpura, splenomegaly, jaundice, microencephaly, mental retardation, meningoencephalitis, radiolucent bone disease.Laboratory confirmation can be obtained by any of the following: virus isolation, serologi test (pasif hemaglutination, latex agglutinationtest, hemaglutination inhibisi, Flouresence immunoassay, Enzyme immunoassay), RNA test.

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13

Siber, Margaret. "X-linked recessive microencephaly, microphthalmia with corneal opacities, spastic quadriplegia, hypospadias and cryptorchidism." Clinical Genetics 26, no. 5 (April 23, 2008): 453–56. http://dx.doi.org/10.1111/j.1399-0004.1984.tb01088.x.

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14

Bonthius, Daniel J., and James R. West. "Blood alcohol concentration and microencephaly: A dose-response study in the neonatal rat." Teratology 37, no. 3 (March 1988): 223–31. http://dx.doi.org/10.1002/tera.1420370307.

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15

Reamy, Amanda A., and Michael J. Wolfgang. "Carnitine palmitoyltransferase-1c gain-of-function in the brain results in postnatal microencephaly." Journal of Neurochemistry 118, no. 3 (June 17, 2011): 388–98. http://dx.doi.org/10.1111/j.1471-4159.2011.07312.x.

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16

Tang, Bor Luen. "Zika virus as a causative agent for primary microencephaly: the evidence so far." Archives of Microbiology 198, no. 7 (July 13, 2016): 595–601. http://dx.doi.org/10.1007/s00203-016-1268-7.

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17

Garg, Divyani, Ayush Agarwal, and Sangeeta Agarwal. "Microencephaly in macrocephaly: Rare report of two siblings with glutaric aciduria type 1." Annals of Movement Disorders 4, no. 1 (2021): 42. http://dx.doi.org/10.4103/aomd.aomd_4_20.

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18

Watanabe, Masayuki, Yoshio Kodama, Yoko Hagino, Ryo-ichi Nonaka, and Yasusuke Kaichi. "Effect of chronic amitriptyline administration on serotonergic receptors in rats with methylazoxymethanol-induced microencephaly." Brain Research 787, no. 2 (March 1998): 333–36. http://dx.doi.org/10.1016/s0006-8993(97)01489-3.

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19

McFarland, K. N., S. R. Wilkes, S. E. Koss, K. S. Ravichandran, and J. W. Mandell. "Neural-Specific Inactivation of ShcA Results in Increased Embryonic Neural Progenitor Apoptosis and Microencephaly." Journal of Neuroscience 26, no. 30 (July 26, 2006): 7885–97. http://dx.doi.org/10.1523/jneurosci.3524-05.2006.

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20

Kozlowski, P. B., J. Brudkowska, M. Kraszpulski, E. A. Sersen, M. A. Wrzolek, A. P. Anzil, C. Rao, and H. M. Wisniewski. "Microencephaly in children congenitally infected with human immunodeficiency virus - a gross-anatomical morphometric study." Acta Neuropathologica 93, no. 2 (February 24, 1997): 136–45. http://dx.doi.org/10.1007/s004010050594.

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21

Karacay, Bahri, Jo Mahoney, Jeffrey Plume, and Daniel J. Bonthius. "Genetic Absence of nNOS Worsens Fetal Alcohol Effects in Mice. II: Microencephaly and Neuronal Losses." Alcoholism: Clinical and Experimental Research 39, no. 2 (February 2015): 221–31. http://dx.doi.org/10.1111/acer.12615.

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22

Haydar, Tarik F., Richard S. Nowakowski, Paul J. Yarowsky, and Bruce K. Krueger. "Role of Founder Cell Deficit and Delayed Neuronogenesis in Microencephaly of the Trisomy 16 Mouse." Journal of Neuroscience 20, no. 11 (June 1, 2000): 4156–64. http://dx.doi.org/10.1523/jneurosci.20-11-04156.2000.

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23

Hecht, W., C. Herden, and A. Herrmann. "Lissencephaly and microencephaly combined with hypoplasia of corpus callosum and cerebellum in a domestic cat." Tierärztliche Praxis Ausgabe K: Kleintiere / Heimtiere 39, no. 02 (2011): 116–20. http://dx.doi.org/10.1055/s-0038-1623564.

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24

Xiao Xia Tan and Lucio G. Costa. "Long-lasting microencephaly following exposure to cocaine during the brain growth spurt in the rat." Developmental Brain Research 84, no. 2 (February 1995): 179–84. http://dx.doi.org/10.1016/0165-3806(94)00169-z.

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25

Pierce, Dwight R., and James R. West. "Alcohol-induced microencephaly during the third trimester equivalent: Relationship to dose and blood alcohol concentration." Alcohol 3, no. 3 (May 1986): 185–91. http://dx.doi.org/10.1016/0741-8329(86)90043-1.

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26

Chen, Wei-Jung A., Robert E. McAlhany, and James R. West. "4-Methylpyrazole, an alcohol dehydrogenase inhibitor, exacerbates alcohol-induced microencephaly during the brain growth spurt." Alcohol 12, no. 4 (July 1995): 351–55. http://dx.doi.org/10.1016/0741-8329(95)00017-l.

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27

PENG, Y., K. KWOK, P. YANG, S. NG, J. LIU, O. WONG, M. HE, H. KUNG, and M. LIN. "Ascorbic acid inhibits ROS production, NF-?B activation and prevents ethanol-induced growth retardation and microencephaly." Neuropharmacology 48, no. 3 (March 2005): 426–34. http://dx.doi.org/10.1016/j.neuropharm.2004.10.018.

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28

Di Luca, M., M. Cimino, P. N. E. De Graan, A. B. Oestreicher, W. H. Gispen, and F. Cattabeni. "Microencephaly reduces the phosphorylation of the PKC substrate B-50/GAP43 in rat cortex and hippocampus." Brain Research 538, no. 1 (January 1991): 95–101. http://dx.doi.org/10.1016/0006-8993(91)90381-5.

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29

Okoshi, Yumi, Masaharu Hayashi, Sachiko Kanda, and Toshiyuki Yamamoto. "An autopsy case of microencephaly, bizarre putaminal lesion, and cerebellar atrophy with heart and liver diseases." Brain and Development 36, no. 8 (September 2014): 707–10. http://dx.doi.org/10.1016/j.braindev.2013.11.010.

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30

Krieger, Teresa G., Carla M. Moran, Alberto Frangini, W. Edward Visser, Erik Schoenmakers, Francesco Muntoni, Chris A. Clark, et al. "Mutations in thyroid hormone receptor α1 cause premature neurogenesis and progenitor cell depletion in human cortical development." Proceedings of the National Academy of Sciences 116, no. 45 (October 18, 2019): 22754–63. http://dx.doi.org/10.1073/pnas.1908762116.

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Mutations in the thyroid hormone receptor α 1 gene (THRA) have recently been identified as a cause of intellectual deficit in humans. Patients present with structural abnormalities including microencephaly, reduced cerebellar volume and decreased axonal density. Here, we show that directed differentiation of THRA mutant patient-derived induced pluripotent stem cells to forebrain neural progenitors is markedly reduced, but mutant progenitor cells can generate deep and upper cortical layer neurons and form functional neuronal networks. Quantitative lineage tracing shows that THRA mutation-containing progenitor cells exit the cell cycle prematurely, resulting in reduced clonal output. Using a micropatterned chip assay, we find that spatial self-organization of mutation-containing progenitor cells in vitro is impaired, consistent with down-regulated expression of cell–cell adhesion genes. These results reveal that thyroid hormone receptor α1 is required for normal neural progenitor cell proliferation in human cerebral cortical development. They also exemplify quantitative approaches for studying neurodevelopmental disorders using patient-derived cells in vitro.

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31

Steinbach, Rosemary J., Nicole N. Haese, Jessica L. Smith, Lois M. A. Colgin, Rhonda P. MacAllister, Justin M. Greene, Christopher J. Parkins, et al. "A neonatal nonhuman primate model of gestational Zika virus infection with evidence of microencephaly, seizures and cardiomyopathy." PLOS ONE 15, no. 1 (January 14, 2020): e0227676. http://dx.doi.org/10.1371/journal.pone.0227676.

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32

Bonthius, Daniel J., Georgios Tzouras, Bahri Karacay, Jolonda Mahoney, Ana Hutton, Ross McKim, and Nicholas J. Pantazis. "Deficiency of neuronal nitric oxide synthase (nNOS) worsens alcohol-induced microencephaly and neuronal loss in developing mice." Developmental Brain Research 138, no. 1 (September 2002): 45–59. http://dx.doi.org/10.1016/s0165-3806(02)00458-3.

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33

Kelly, Sandra J., Dwight R. Pierce, and James R. West. "Microencephaly and hyperactivity in adult rats can be induced by neonatal exposure to high blood alcohol concentrations." Experimental Neurology 96, no. 3 (June 1987): 580–93. http://dx.doi.org/10.1016/0014-4886(87)90220-2.

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34

Bonthius, Daniel J., Charles R. Goodlett, and James R. West. "Blood alcohol concentration and severity of microencephaly in neonatal rats depend on the pattern of alcohol administration." Alcohol 5, no. 3 (May 1988): 209–14. http://dx.doi.org/10.1016/0741-8329(88)90054-7.

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35

Harakawa, Seijiro, Shoichi Akazawa, Mihoko Akazawa, Masumi Hashimoto, Shunichi Yamashita, Motomori Izumi, and Shigenobu Nagataki. "Changes of serum thyroid hormone levels induce malformations on early embryogenesis in rats." Acta Endocrinologica 121, no. 5 (November 1989): 739–43. http://dx.doi.org/10.1530/acta.0.1210739.

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Abstract. The incidence of malformation is increased in infants of hyperthyroid or hypothyroid woman. Although many papers reported that the fetus is insulted from maternal thyroid hormone, the placenta (maternalfetal barrier) is not yet fully developed before 11.5 days of gestation in rat embryos, suggesting the effect of thyroid hormone on early rat embryogenesis. This study was, therefore, undertaken to investigate whether excess or lack of thyroid hormones would affect early embryogenesis in rat embryo culture. Malformations including open neuropore and microencephaly were observed in 10 of 30 embryos incubated in hyperthyroid serum, and in 12 of 42 cultured in T3-enriched normal serum. Similar malformations were observed in 14 of 42 embryos cultured in hypothyroid serum and in 10 of 30 cultured in hypothyroid serum supplemented with T3. The frequencies of these malformations were significantly higher than in the control embryos (0 in 72 embryos) cultured with normal rat serum. These results suggest that the maternal thyroid status might play an important role for the complication of fetal malformations during early gestational period.

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36

Kousa, Youssef A., and Reafa A. Hossain. "Causes of Phenotypic Variability and Disabilities after Prenatal Viral Infections." Tropical Medicine and Infectious Disease 6, no. 2 (June 1, 2021): 95. http://dx.doi.org/10.3390/tropicalmed6020095.

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Prenatal viral infection can lead to a spectrum of neurodevelopmental disabilities or fetal demise. These can include microencephaly, global developmental delay, intellectual disability, refractory epilepsy, deafness, retinal defects, and cortical-visual impairment. Each of these clinical conditions can occur on a semi-quantitative to continuous spectrum, from mild to severe disease, and often as a collective of phenotypes. Such serious outcomes result from viruses’ overlapping neuropathology and hosts’ common neuronal and gene regulatory response to infections. The etiology of variability in clinical outcomes is not yet clear, but it may be related to viral, host, vector, and/or environmental risk and protective factors that likely interact in multiple ways. In this perspective of the literature, we work toward understanding the causes of phenotypic variability after prenatal viral infections by highlighting key aspects of the viral lifecycle that can affect human disease, with special attention to the 2015 Zika pandemic. Therefore, this work offers important insights into how viral infections and environmental teratogens affect the prenatal brain, toward our ultimate goal of preventing neurodevelopmental disabilities.

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37

Forni, P. E. "High Levels of Cre Expression in Neuronal Progenitors Cause Defects in Brain Development Leading to Microencephaly and Hydrocephaly." Journal of Neuroscience 26, no. 37 (September 13, 2006): 9593–602. http://dx.doi.org/10.1523/jneurosci.2815-06.2006.

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38

Oka, C., T. Nakano, A. Wakeham, J. L. de la Pompa, C. Mori, T. Sakai, S. Okazaki, et al. "Disruption of the mouse RBP-J kappa gene results in early embryonic death." Development 121, no. 10 (October 1, 1995): 3291–301. http://dx.doi.org/10.1242/dev.121.10.3291.

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The RBP-J kappa protein is a transcription factor that recognizes the sequence C(T)GTGGGGA. The RBP-J kappa gene is highly conserved in a wide variety of species and the Drosophila homologue has been shown to be identical to Suppressor of Hairless [Su(H)] which plays important roles in the development of the peripheral nervous system. To explore the function of the RBP-J kappa gene in mouse embryogenesis, a mutation was introduced into the functional RBP-J kappa gene in embryonic stem (ES) cells by homologous recombination. Null mutant ES cells survived but null mutant mice showed embryonic lethality before 10.5 days of gestation. The mutant mice showed severe growth retardation as early as 8.5 days of gestation. Developmental abnormalities, including incomplete turning of the body axis, microencephaly, abnormal placental development, anterior neuropore opening and defective somitogenesis, were observed in the mutant mice at 9.5 days of gestation. RBP-J kappa mutant embryos expressed a posterior mesodermal marker FGFR1. Their irregularly shaped somites expressed a somite marker gene Mox 1 but failed to express myogenin. The RBP-J kappa gene was revealed to be essential for postimplantation development of mice.

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39

Chen, Wei-Jung A., Kathleen H. Andersen, and James R. West. "Alcohol-induced brain growth restrictions (microencephaly) were not affected by concurrent exposure to cocaine during the brain growth spurt." Teratology 50, no. 3 (September 1994): 250–55. http://dx.doi.org/10.1002/tera.1420500310.

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40

Robertson, Richard T., Thomas G. Gragnola, and Jen Yu. "Patterns of transiently expressed acetylcholinesterase activity in cerebral cortex and dorsal thalamus of developing rats with cytotoxin-induced microencephaly." International Journal of Developmental Neuroscience 8, no. 2 (1990): 223–32. http://dx.doi.org/10.1016/0736-5748(90)90015-t.

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41

Plume, Jeffrey M., Dylan Todd, and Daniel J. Bonthius. "Viral Strain Determines Disease Symptoms, Pathology, and Immune Response in Neonatal Rats with Lymphocytic Choriomeningitis Virus Infection." Viruses 11, no. 6 (June 14, 2019): 552. http://dx.doi.org/10.3390/v11060552.

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When infection with lymphocytic choriomeningitis (LCMV) occurs during pregnancy, the virus can infect the fetus and injure the fetal brain. However, type, location, and severity of neuropathology differ among cases. One possible explanation for this diversity is that fetuses are infected with different viral strains. Using a rat model of congenital LCMV infection, we investigated how differences in LCMV strain (E350, WE2.2, and Clone 13) affect outcome. Rat pups received intracranial inoculations on postnatal day 4. E350 initially targeted glial cells, while WE2.2 and Clone 13 targeted neurons. The E350 strain induced focal destructive lesions, while the other strains induced global microencephaly. E350 attracted large numbers of CD8+ lymphocytes early in the disease course, while Clone 13 attracted CD4+ lymphocytes, and the infiltration occurred late. The E350 and WE2.2 strains induced large increases in expression of pro-inflammatory cytokines, while Clone 13 did not. The animals infected with E350 and WE2.2 became ataxic and performed poorly on the negative geotaxis assay, while the Clone 13 animals had profound growth failure. Thus, in the developing brain, different LCMV strains have different patterns of infection, neuropathology, immune responses and disease symptoms. In humans, different outcomes from congenital LCMV may reflect infection with different strains.

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42

Pierce, D. R., C. J. M. Kane, D. C. Serbus, and K. E. Light. "Microencephaly and Selective Decreases in Cerebellar Purkinje Cell Numbers Following Combined Exposure to Ethanol and Methadone during Rat Brain Development." Developmental Neuroscience 19, no. 5 (1997): 438–45. http://dx.doi.org/10.1159/000111241.

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43

Koh, Sookyong, Tatiane C. Santos, and Andrew J. Cole. "Susceptibility to seizure-induced injury and acquired microencephaly following intraventricular injection of saporin-conjugated 192 IgG in developing rat brain." Experimental Neurology 194, no. 2 (August 2005): 457–66. http://dx.doi.org/10.1016/j.expneurol.2005.03.002.

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44

Jeneetta Jose, Rasmi S Nair, and Meenu Vijayan. "A review on zika virus: clinical aspects and therapeutic responses." International Journal of Research in Pharmaceutical Sciences 11, no. 4 (November 9, 2020): 6646–53. http://dx.doi.org/10.26452/ijrps.v11i4.3578.

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The Zika Virus (ZIKV) happens to be one of the recent infections investigated after the Ebola pandemic. It is an arthropod-borne virus (arbovirus) within the family Flaviviridae class. ZIKV is an RNA virus with a single strand, enveloped, icosahedral, non-sectioned, positive sense. It is 40 nm wide and has an outer (E) envelope and a dense inner core. The ZIKV can be transmitted by two methods: human and human-to-human vectors. The vector transmission is by Aedes spp. Mosquitoes and diseases outside Africa are transmitted by Aedes aegypti. Originating in Nigeria in 1947 it was reported as a mild illness and from a rhesus monkey. With a certain passage of time earned significant attention from healthcare organisations for the human population. Many clinical symptoms in adults in French Polynesia have been recorded, ranging from mild illness to severe neurological problems such as Guillain-Barré syndrome. Other symptoms include encephalitis microencephaly, meningoencephalitis, myelitis, paraesthesia, vertigo, facial and ophthalmological paralysis (photophobia and hypertensive iridocyclitis) and auditory manifestations. In this review, the clinical aspects and other therapeutic responses are studied here to understand the approach more treating symptoms arising with the infection of the Zika virus. Various complications have been studied in this review and diagnosis have been performed to identify the presence in the human body and also take clinical measures on alleviating the symptoms of the infected patients.

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45

Tessel, Richard E., Pippa S. Loupe, Stephen R. Schroeder, and John Schloss. "Kinetic assessment of the effects of task difficulty, microencephaly, and a response manipulandum alteration on the rate of fixed-ratio discrimination acquisition." Experimental and Clinical Psychopharmacology 10, no. 4 (2002): 408–16. http://dx.doi.org/10.1037/1064-1297.10.4.408.

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46

Vermehren-Schmaedick, Anke, Jeffrey Y. Huang, Madison Levinson, Matthew B. Pomaville, Sarah Reed, Gary A. Bellus, Fred Gilbert, et al. "Characterization of PARP6 Function in Knockout Mice and Patients with Developmental Delay." Cells 10, no. 6 (May 22, 2021): 1289. http://dx.doi.org/10.3390/cells10061289.

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PARP6, a member of a family of enzymes (17 in humans) known as poly-ADP-ribose polymerases (PARPs), is a neuronally enriched PARP. While previous studies from our group show that Parp6 is a regulator of dendrite morphogenesis in rat hippocampal neurons, its function in the nervous system in vivo is poorly understood. Here, we describe the generation of a Parp6 loss-of-function mouse model for examining the function of Parp6 during neurodevelopment in vivo. Using CRISPR-Cas9 mutagenesis, we generated a mouse line that expressed a Parp6 truncated variant (Parp6TR) in place of Parp6WT. Unlike Parp6WT, Parp6TR is devoid of catalytic activity. Homozygous Parp6TR do not exhibit obvious neuromorphological defects during development, but nevertheless die perinatally. This suggests that Parp6 catalytic activity is important for postnatal survival. We also report PARP6 mutations in six patients with several neurodevelopmental disorders, including microencephaly, intellectual disabilities, and epilepsy. The most severe mutation in PARP6 (C563R) results in the loss of catalytic activity. Expression of Parp6C563R in hippocampal neurons decreases dendrite morphogenesis. To gain further insight into PARP6 function in neurons we also performed a BioID proximity labeling experiment in hippocampal neurons and identified several microtubule-binding proteins (e.g., MAP-2) using proteomics. Taken together, our results suggest that PARP6 is an essential microtubule-regulatory gene in mice, and that the loss of PARP6 catalytic activity has detrimental effects on neuronal function in humans.

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de Licona, Hannah Klein, Bahri Karacay, Jo Mahoney, Elizabeth McDonald, Thirath Luang, and Daniel J. Bonthius. "A single exposure to alcohol during brain development induces microencephaly and neuronal losses in genetically susceptible mice, but not in wild type mice." NeuroToxicology 30, no. 3 (May 2009): 459–70. http://dx.doi.org/10.1016/j.neuro.2009.01.010.

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Costa, Lucio G., Gennaro Giordano, and Marina Guizzetti. "Inhibition of cholinergic muscarinic signaling by ethanol: Potential mechanism of developmental neurotoxicity and biological plausibility for the beneficial effects of choline supplementation." International Journal of Alcohol and Drug Research 2, no. 3 (March 20, 2013): 17–25. http://dx.doi.org/10.7895/ijadr.v2i3.72.

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Costa, L., Giordano, G., & Guizzetti, M. (2013). Inhibition of cholinergic muscarinic signaling by ethanol: Potential mechanism of developmental neurotoxicity and biological plausibility for the beneficial effects of choline supplementation. The International Journal Of Alcohol And Drug Research, 2(3), 17-25. doi:10.7895/ijadr.v2i3.72 (http://dx.doi.org/10.7895/ijadr.v2i3.72)Central nervous system dysfunctions are among the most significant effects of in utero exposure to ethanol. Ethanol has been shown to affect neurons and glial cells, causing cell loss and impaired cell migration and maturation. Multiple mechanisms have been suggested to underlie the effects of ethanol, including interference with growth factors, cytokines, cell adhesion molecules and neurotransmitters. Here, we propose that a relevant mechanism of ethanol’s developmental neurotoxicity may be its ability to inhibit the actions of acetylcholine in the developing nervous system mediated by activation of cholinergic muscarinic receptors. Acetylcholine has been shown to induce proliferation of astrocytes, to protect neurons against apoptotic cell death, and to foster astrocyte-neuronal interactions, thereby increasing neuritogenesis. By interfering with muscarinic receptor signal transduction pathways (mostly at the level of phospholipase D), ethanol inhibits all these effects of acetylcholine in the developing brain. Such action of ethanol may be responsible, at least in part, for some manifestations of developmental neurotoxicity, such as microencephaly, neuronal cell death and impaired neuronal differentiation. Among potential therapeutic interventions for fetal alcohol spectrum disorders, choline supplementation appears to be one of the most promising. The cholinergic hypothesis of ethanol’s developmental neurotoxicity provides biological plausibility for the beneficial effects of choline. Indeed, by “potentiating” the cholinergic system during development (through increased synthesis of acetylcholine and phosphatidylcholine, and increased phospholipase D activity), choline would antagonize at least some of the deleterious effects of ethanol.

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Maier, Susan E., Wei-Jung A. Chen, Jennifer A. Miller, and James R. West. "Fetal Alcohol Exposure and Temporal Vulnerability: Regional Differences in Alcohol-Induced Microencephaly as a Function of the Timing of Binge-Like Alcohol Exposure During Rat Brain Development." Alcoholism: Clinical and Experimental Research 21, no. 8 (November 1997): 1418–25. http://dx.doi.org/10.1111/j.1530-0277.1997.tb04471.x.

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Ueda, Shuichi, Kanji Yoshimoto, Taro Kadowaki, Koichi Hirata, and Shin-ichi Sakakibara. "Improved learning in microencephalic rats." Congenital Anomalies 50, no. 1 (March 2010): 58–63. http://dx.doi.org/10.1111/j.1741-4520.2009.00265.x.

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