Cortical deficits of glutamic acid decarboxylase 67 expression in schizophrenia: clinical, protein, and cell type-specific features.
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OBJECTIVE: Cognitive deficits in schizophrenia are associated with altered activity of the dorsolateral prefrontal cortex, which has been attributed to lower expression of the 67 kDa isoform of glutamic acid decarboxylase (GAD67), the major γ-aminobutyric acid (GABA)-synthesizing enzyme. However, little is known about the relationship of prefrontal GAD67 mRNA levels and illness severity, translation of the transcript into protein, and protein levels in axon terminals, the key site of GABA production and function. METHOD: Quantitative polymerase chain reaction was used to measure GAD67 mRNA levels in postmortem specimens of dorsolateral prefrontal cortex from subjects with schizophrenia and matched comparison subjects with no known history of psychiatric or neurological disorders (N=42 pairs). In a subset of this cohort in which potential confounds of protein measures were controlled (N=19 pairs), Western blotting was used to quantify tissue levels of GAD67 protein in tissue. In five of these pairs, multilabel confocal immunofluorescence was used to quantify GAD67 protein levels in the axon terminals of parvalbumin-containing GABA neurons, which are known to have low levels of GAD67 mRNA in schizophrenia. RESULTS: GAD67 mRNA levels were significantly lower in schizophrenia subjects (by 15%), but transcript levels were not associated with predictors or measures of illness severity or chronicity. In schizophrenia subjects, GAD67 protein levels were significantly lower in total gray matter (by 10%) and in parvalbumin axon terminals (by 49%). CONCLUSIONS: The findings that lower GAD67 mRNA expression is common in schizophrenia, that it is not a consequence of having the illness, and that it leads to less translation of the protein, especially in the axon terminals of parvalbumin-containing neurons, support the hypothesis that lower GABA synthesis in parvalbumin neurons contributes to dorsolateral prefrontal cortex dysfunction and impaired cognition in schizophrenia.
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Reduced PV and GAD67 protein levels are seen in both prefrontal and temporal cortex of post-mortem brain tissues from schizophrenia patients.
“Reduced PV and GAD67 protein levels are also seen in both prefrontal and temporal cortex of post-mortem brain tissues (Beasley and Reynolds, 1997; Curley et al., 2011; Glausier et al., 2014).”
From The Perineuronal ‘Safety’ Net? Perineuronal Net Abnormalities in Neurological Disorders (2018) · cites this paper as Curley et al., 2011
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Cites
An Integrative Theory of Prefrontal Cortex Function
Miller, E. K., & Cohen, J. D. (2001) · Annual Review of Neuroscience · doi:10.1146/annurev.neuro.24.1.167 · Cited by 12,803 · see citing works
Two Factor Index of Social Position
Hollingshead, A. B. (1957) · Cited by 3,757 · see citing works
What are the functional consequences of neurocognitive deficits in schizophrenia?
(1996) · American Journal of Psychiatry · doi:10.1176/ajp.153.3.321 · Cited by 3,516 · see citing works
Driving fast-spiking cells induces gamma rhythm and controls sensory responses
Cardin, J. A., Carlén, M., Meletis, K., Knoblich, U., Zhang, F., Deisseroth, K., Tsai, L.-H., & Moore, C. I. (2009) · Nature · doi:10.1038/nature08002 · Cited by 2,603 · see citing works
Cortical inhibitory neurons and schizophrenia
Lewis, D. A., Hashimoto, T., & Volk, D. W. (2005) · Nature Reviews Neuroscience · doi:10.1038/nrn1648 · Cited by 2,297 · see citing works
Self-citationPhysiologic Dysfunction of Dorsolateral Prefrontal Cortex in Schizophrenia
Weinberger, D. R. (1986) · Archives of General Psychiatry · doi:10.1001/archpsyc.1986.01800020020004 · Cited by 2,019 · see citing works
Guidotti, A., Auta, J., Davis, J. M., Gerevini, V. D. G., Dwivedi, Y., Grayson, D. R., Impagnatiello, F., Pandey, G. N., Pesold, C., Sharma, R. P., et al. (2000) · Archives of General Psychiatry · doi:10.1001/archpsyc.57.11.1061 · Cited by 1,203 · see citing works
Meta-analysis of 41 functional neuroimaging studies of executive function in schizophrenia
Minzenberg, M. J., Laird, A. R., Thelen, S., Carter, C. S., & Glahn, D. C. (2009) · Archives of General Psychiatry · doi:10.1001/archgenpsychiatry.2009.91 · Cited by 1,158 · see citing works
Akbarian, S. (1995) · Archives of General Psychiatry · doi:10.1001/archpsyc.1995.03950160008002 · Cited by 1,002 · see citing works
Hashimoto, T., Volk, D. W., Eggan, S. M., Mirnics, K., Pierri, J. N., Sun, Z., Sampson, A. R., & Lewis, D. A. (2003) · The Journal of Neuroscience · doi:10.1523/jneurosci.23-15-06315.2003 · Cited by 938 · see citing works
Self-citationInduced γ-Band Activity during the Delay of a Visual Short-Term Memory Task in Humans
Tallon‐Baudry, C., Bertrand, O., Peronnet, F., & Pernier, J. (1998) · Journal of Neuroscience · doi:10.1523/jneurosci.18-11-04244.1998 · Cited by 900 · see citing works
Volk, D. W., Austin, M. C., Pierri, J. N., Sampson, A. R., & Lewis, D. A. (2000) · Archives of General Psychiatry · doi:10.1001/archpsyc.57.3.237 · Cited by 697 · see citing works
Self-citationImpairments in frontal cortical γ synchrony and cognitive control in schizophrenia
CHO, R. Y., Konecky, R. O., & Carter, C. S. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0609440103 · Cited by 576 · see citing works
González‐Burgos, G., & Lewis, D. A. (2008) · Schizophrenia Bulletin · doi:10.1093/schbul/sbn070 · Cited by 568 · see citing works
Self-citationAsada, H., Kawamura, Y., Maruyama, K., Kume, H., Ding, R.-G., Kanbara, N., Kuzume, H., Sanbo, M., Yagi, T., & Obata, K. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.12.6496 · Cited by 556 · see citing works
Imbeaud, S. (2005) · Nucleic Acids Research · doi:10.1093/nar/gni054 · Cited by 530 · see citing works
Cognitive Control Deficits in Schizophrenia: Mechanisms and Meaning
Lesh, T. A., Niendam, T. A., Minzenberg, M., & Carter, C. S. (2010) · Neuropsychopharmacology · doi:10.1038/npp.2010.156 · Cited by 495 · see citing works
Hashimoto, T., Arion, D., Unger, T., Maldonado-Avilés, J. G., Morris, H. M., Volk, D. W., Mirnics, K., & Lewis, D. A. (2008) · Molecular Psychiatry · doi:10.1038/sj.mp.4002011 · Cited by 490 · see citing works
Self-citationHashimoto, T., Bazmi, H. H., Mirnics, K., Wu, Q., Sampson, A. R., & Lewis, D. A. (2008) · American Journal of Psychiatry · doi:10.1176/appi.ajp.2007.07081223 · Cited by 457 · see citing works
Self-citationYoon, J. H., Maddock, R. J., Rokem, A., Silver, M. A., Minzenberg, M. J., Ragland, J. D., & Carter, C. S. (2010) · The Journal of Neuroscience · doi:10.1523/jneurosci.6158-09.2010 · Cited by 408 · see citing works
How should DSM-V criteria for schizophrenia include cognitive impairment?
Keefe, R. S. E., & Fenton, W. S. (2007) · Schizophrenia Bulletin · doi:10.1093/schbul/sbm046 · Cited by 394 · see citing works
Hashimoto, T., Bergen, S. E., Nguyen, Q. L., Xu, B., Monteggia, L. M., Pierri, J. N., Sun, Z., Sampson, A. R., & Lewis, D. A. (2005) · Journal of Neuroscience · doi:10.1523/jneurosci.4035-04.2005 · Cited by 384 · see citing works
Self-citationAsada, H., Kawamura, Y., Maruyama, K., Kume, H., Ding, R.-G., Ji, F. Y., Kanbara, N., Kuzume, H., Sanbo, M., Yagi, T., et al. (1996) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.1996.1898 · Cited by 315 · see citing works
Reduced Dendritic Spine Density in Auditory Cortex of Subjects with Schizophrenia
Sweet, R. A., Henteleff, R. A., Zhang, W., Sampson, A. R., & Lewis, D. A. (2009) · Neuropsychopharmacology · doi:10.1038/npp.2008.67 · Cited by 290 · see citing works
Self-citationAlterations of cortical GABA neurons and network oscillations in schizophrenia
Gonzalez-Burgos, G., Hashimoto, T., & Lewis, D. A. (2010) · Current Psychiatry Reports · doi:10.1007/s11920-010-0124-8 · Cited by 260 · see citing works
Minzenberg, M. J., Firl, A. J., Yoon, J. H., Gomes, G. C., Reinking, C., & Carter, C. S. (2010) · Neuropsychopharmacology · doi:10.1038/npp.2010.150 · Cited by 247 · see citing works
Reduced Cortical Cannabinoid 1 Receptor Messenger RNA and Protein Expression in Schizophrenia
Eggan, S. M., Hashimoto, T., & Lewis, D. A. (2008) · Archives of General Psychiatry · doi:10.1001/archpsyc.65.7.772 · Cited by 219 · see citing works
Self-citationEnomoto, T., Tse, M. T., & Floresco, S. B. (2011) · Biological Psychiatry · doi:10.1016/j.biopsych.2010.09.038 · Cited by 179 · see citing works
Pigments in Aging: An Overview
Porta, E. A. (2002) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2002.tb02083.x · Cited by 173 · see citing works
Elevated Gamma-Aminobutyric Acid Levels in Chronic Schizophrenia
Öngür, D., Prescot, A. P., McCarthy, J. M., Cohen, B. M., & Renshaw, P. F. (2010) · Biological Psychiatry · doi:10.1016/j.biopsych.2010.05.016 · Cited by 144 · see citing works
Activity-dependent Changes in GAD and Preprotachykinin mRNAs in Visual Cortex of Adult Monkeys
Benson, D. L., Huntsman, M. M., & Jones, E. G. (1994) · Cerebral Cortex · doi:10.1093/cercor/4.1.40 · Cited by 133 · see citing works
Evidence that GAD65 mediates increased GABA synthesis during intense neuronal activity in vivo
Patel, A. B., de Graaf, R. A., Martin, D. L., Battaglioli, G., & Behar, K. L. (2006) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2006.03741.x · Cited by 124 · see citing works
Sawaguchi, T., Matsumura, M., & Kubota, K. (1989) · Experimental Brain Research · doi:10.1007/bf00249897 · Cited by 109 · see citing works
Benes, F. M., Todtenkopf, M. S., Logiotatos, P., & Williams, M. (2000) · Journal of Chemical Neuroanatomy · doi:10.1016/s0891-0618(00)00105-8 · Cited by 109 · see citing works
Nelson, P. T., & Keller, J. N. (2007) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/01.jnen.0000240474.27791.f3 · Cited by 108 · see citing works
Gotō, N., Yoshimura, R., Moriya, J., Kakeda, S., Ueda, N., Ikenouchi, A., Umene‐Nakano, W., Hayashi, K., Oonari, N., Korogi, Y., et al. (2009) · Schizophrenia Research · doi:10.1016/j.schres.2009.04.026 · Cited by 88 · see citing works
Mason, G. F., Martin, D. L., Martin, S. B., Manor, D., Sibson, N. R., Patel, A. B., Rothman, D. L., & Behar, K. L. (2001) · Brain Research · doi:10.1016/s0006-8993(01)02778-0 · Cited by 85 · see citing works
Rimvall, K., Sheikh, S. N., & Martin, D. L. (1993) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.1993.tb03206.x · Cited by 74 · see citing works
Fish, K. N., Sweet, R. A., Deo, A. J., & Lewis, D. A. (2008) · Brain Research · doi:10.1016/j.brainres.2008.08.060 · Cited by 43 · see citing works
Self-citationNeurobiology of Mental Illness
Anderson, K. E. (2005) · The Journal of Nervous and Mental Disease · doi:10.1097/01.nmd.0000152830.28345.3c · Cited by 27 · see citing works
Gotō, N., Yoshimura, R., Kakeda, S., Moriya, J., Hayashi, K., Ikenouchi, A., Umene‐Nakano, W., Hori, H., Ueda, N., Korogi, Y., et al. (2009) · Human Psychopharmacology Clinical and Experimental · doi:10.1002/hup.1070 · Cited by 27 · see citing works
Human Postmortem Brain Research in Mental Illness Syndromes
Beneyto, M., Sibille, E. L., & Lewis, D. A. (2011) · Oxford University Press eBooks · doi:10.1093/med/9780199798261.003.0015 · Cited by 11 · see citing works
Self-citation
Flagged first, then by citations
1 of the 43 references couldn’t be matched to a known paper.
Cited by
Sorted by citations
Cortical parvalbumin interneurons and cognitive dysfunction in schizophrenia
Lewis, D. A., Curley, A. A., Glausier, J. R., & Volk, D. W. (2012) · Trends in Neurosciences · doi:10.1016/j.tins.2011.10.004 · Cited by 1,071 · see citing works
Self-citationAlterations in Cortical Network Oscillations and Parvalbumin Neurons in Schizophrenia
Gonzalez-Burgos, G., Cho, R. Y., & Lewis, D. A. (2015) · Biological Psychiatry · doi:10.1016/j.biopsych.2015.03.010 · Cited by 497 · see citing works
“Moreover, lower cortical GAD67 mRNA levels appear to not be a consequence of illness chronicity (103), of factors that are frequently comorbid with schizophrenia, or of medications used to treat the illness (101).”
BackgroundSelf-citationKaar, S., Natesan, S., McCutcheon, R., & Howes, O. (2020) · Neuropharmacology · doi:10.1016/j.neuropharm.2019.107704 · Cited by 348 · see citing works
Erbb4 Deletion from Fast-Spiking Interneurons Causes Schizophrenia-like Phenotypes
del Pino, I., García-Frigola, C., Dehorter, N., Brotons-Mas, J. R., Alvarez-Salvado, E., Martínez de Lagrán, M., Ciceri, G., Gabaldón, M. V., Moratal, D., Dierssen, M., et al. (2013) · Neuron · doi:10.1016/j.neuron.2013.07.010 · Cited by 314 · see citing works
“Loss of GAD67 seems to preferentially affect fast-spiking interneurons (Curley et al., 2011; Hashimoto et al., 2003), which also contain reduced levels of PV (Hashimoto et al., 2003).”
BackgroundAlterations in cortical interneurons and cognitive function in schizophrenia
Dienel, S. J., & Lewis, D. A. (2018) · Neurobiology of Disease · doi:10.1016/j.nbd.2018.06.020 · Cited by 267 · see citing works
Self-citationOskvig, D. B., Elkahloun, A. G., Johnson, K. R., Phillips, T. M., & Herkenham, M. (2012) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2012.01.015 · Cited by 248 · see citing works
“…are believed to result at least partially from an excitation/inhibition imbalance caused by a loss of GABAergic interneurons, supported by the clinical evidence for reduced protein and gene markers for GABAergic interneurons (Curley et al., 2011; Fatemi et al., 2002; Thompson Ray et al., 2011).”
Enwright, J. F., Sanapala, S., Foglio, A., Berry, R., Fish, K. N., & Lewis, D. A. (2016) · Neuropsychopharmacology · doi:10.1038/npp.2016.24 · Cited by 223 · see citing works
“These approaches have been previously used to obtain quantitative measures of immunofluorescence intensity across a wide dynamic range (Curley et al, 2011; Fish et al, 2011; Glausier et al, 2015).”
Self-citationNeurodevelopment, GABA System Dysfunction, and Schizophrenia
Schmidt, M. J., & Mirnics, K. (2014) · Neuropsychopharmacology · doi:10.1038/npp.2014.95 · Cited by 239 · see citing works
Smucny, J., Dienel, S. J., Lewis, D. A., & Carter, C. S. (2022) · Neuropsychopharmacology · doi:10.1038/s41386-021-01089-0 · Cited by 231 · see citing works
Self-citationInhibitory neurons in human cortical circuits: substrate for cognitive dysfunction in schizophrenia
Lewis, D. A. (2014) · Current Opinion in Neurobiology · doi:10.1016/j.conb.2013.11.003 · Cited by 217 · see citing works
“Consistent with these findings, cortical GAD67 protein levels are also lower in schizophrenia [2;3].”
ResultSelf-citationDevelopmental origins of brain disorders: roles for dopamine
Money, K. M., & Stanwood, G. D. (2013) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2013.00260 · Cited by 221 · see citing works
“Developmental alterations in dendritic growth and/or GABAergic interneuron migration likely contribute to the development of pathology in these disorders (Beasley and Reynolds, 1997; Kaufmann and Moser, 2000; Black et al., 2004; Curley et al., 2011).”
BackgroundCanetta, S., Bolkan, S., Padilla-Coreano, N., Song, L. J., Sahn, R., Harrison, N. L., Gordon, J. A., Brown, A., & Kellendonk, C. (2016) · Molecular Psychiatry · doi:10.1038/mp.2015.222 · Cited by 201 · see citing works
Tatti, R., Haley, M. S., Swanson, O. K., Tselha, T., & Maffei, A. (2016) · Biological Psychiatry · doi:10.1016/j.biopsych.2016.09.017 · Cited by 211 · see citing works
The neurobiology and treatment of first-episode schizophrenia
Kahn, R. S., & Sommer, I. E. (2015) · Molecular Psychiatry · doi:10.1038/mp.2014.66 · Cited by 219 · see citing works
Cannabis-associated psychosis: Neural substrate and clinical impact
Murray, R. M., Englund, A., Abi‐Dargham, A., Lewis, D. A., Forti, M. D., Davies, C., Sherif, M. A., McGuire, P. K., & D’Souza, D. C. (2017) · Neuropharmacology · doi:10.1016/j.neuropharm.2017.06.018 · Cited by 201 · see citing works
“In addition, lower mRNA and protein expression of the GABA synthesizing enzyme GAD67, one of the most consistently reported findings in postmortem studies of schizophrenia (Akbarian et al., 1995; Curley et al., 2011; Duncan et al., 2010; Guidotti et al., 2000; Straub et al., 2007; Volk et al., 2000), could lead to def…”
Self-citationHigh-frequency oscillations and the neurobiology of schizophrenia
Uhlhaas, P. J., & Singer, W. (2013) · Dialogues in Clinical Neuroscience · doi:10.31887/dcns.2013.15.3/puhlhaas · Cited by 196 · see citing works
“In this context it is noteworthy that the messenger RNA for the enzyme GAD 67 which synthesizes GABA is reduced in several cortical areas in SCZ patients.(64) Moreover, this decrease is accompanied by reduced expression of the GABA membrane transporter 1 (GAT1).”
BackgroundSchizophrenia: from neurochemistry to circuits, symptoms and treatments
Howes, O., Bukala, B., & Beck, K. (2023) · Nature Reviews Neurology · doi:10.1038/s41582-023-00904-0 · Cited by 136 · see citing works
“These findings, together with the evidence of lower levels of proteins involved in the production and reuptake of GABA 60,61 , suggest lower cortical GABA levels in schizophrenia relative to healthy individuals.”
Wnt Signaling: Role in Alzheimer Disease and Schizophrenia
Inestrosa, N. C., Montecinos-Oliva, C., & Fuenzalida, M. (2012) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-012-9417-5 · Cited by 186 · see citing works
“Postmortem studies have found reduced levels of glutamic acid decarboxylase (GAD67), a major determinant of GABA levels, in dorsolateral prefrontal cortex of patients with SZ (Curley et al. 2011).”
BackgroundThe Perineuronal ‘Safety’ Net? Perineuronal Net Abnormalities in Neurological Disorders
Wen, T. H., Binder, D. K., Ethell, I. M., & Razak, K. A. (2018) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2018.00270 · Cited by 170 · see citing works
“Reduced PV and GAD67 protein levels are also seen in both prefrontal and temporal cortex of post-mortem brain tissues (Beasley and Reynolds, 1997; Curley et al., 2011; Glausier et al., 2014).”
BackgroundGABAergic Mechanisms in Schizophrenia: Linking Postmortem and In Vivo Studies
de Jonge, J. C., Vinkers, C. H., Pol, H. E. H., & Marsman, A. (2017) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2017.00118 · Cited by 185 · see citing works
“J Neurophysiol (2003) 90(4): 2690–701.”
BackgroundInfluentialThe regulation of glutamic acid decarboxylases in GABA neurotransmission in the brain
Lee, S. E., Lee, Y., & Lee, G. H. (2019) · Archives of Pharmacal Research · doi:10.1007/s12272-019-01196-z · Cited by 171 · see citing works
Perinatal Choline Effects on Neonatal Pathophysiology Related to Later Schizophrenia Risk
Ross, R. G., Hunter, S. K., McCarthy, L., Beuler, J., Hutchison, A. K., Wagner, B. D., Leonard, S., Stevens, K. E., & Freedman, R. (2013) · American Journal of Psychiatry · doi:10.1176/appi.ajp.2012.12070940 · Cited by 165 · see citing works
“Abnormalities in the development of cerebral inhibitory neurons are a key pathophysiological defect in schizophrenia (16).”
BackgroundChung, D. W., Fish, K. N., & Lewis, D. A. (2016) · American Journal of Psychiatry · doi:10.1176/appi.ajp.2016.16010025 · Cited by 148 · see citing works
“Consistent with this hypothesis, postmortem studies have repeatedly shown lower PV and GAD67 levels in the DLPFC of schizophrenia subjects(13-17), which are thought to reflect lower glutamatergic drive to a subset of PV neurons and not a loss of PV neurons in the illness(13, 15, 18, 19).”
BackgroundResultSelf-citationDeficits in Transcriptional Regulators of Cortical Parvalbumin Neurons in Schizophrenia
Volk, D. W., Matsubara, T., Li, S., Sengupta, E. J., Георгиев, Д., Minabe, Y., Sampson, A. R., Hashimoto, T., & Lewis, D. A. (2012) · American Journal of Psychiatry · doi:10.1176/appi.ajp.2012.12030305 · Cited by 155 · see citing works
“To control for experimental variance, subjects with schizophrenia or schizoaffective disorder (N=42) were matched individually to one comparison subject for sex and as closely as possible for age (see Table S1 in the data supplement that accompanies the online edition of this article), as previously described (6, 26,…”
MethodSelf-citationGlausier, J. R., Fish, K. N., & Lewis, D. A. (2014) · Molecular Psychiatry · doi:10.1038/mp.2013.152 · Cited by 147 · see citing works
Self-citationHoftman, G. D., Volk, D. W., Bazmi, H. H., Li, S., Sampson, A. R., & Lewis, D. A. (2013) · Schizophrenia Bulletin · doi:10.1093/schbul/sbt178 · Cited by 146 · see citing works
Self-citationMolina, J. L., Voytek, B., Thomas, M. L., Joshi, Y. B., Bhakta, S. G., Talledo, J., Swerdlow, N. R., & Light, G. A. (2020) · Biological Psychiatry Cognitive Neuroscience and Neuroimaging · doi:10.1016/j.bpsc.2020.02.004 · Cited by 153 · see citing works
McNally, J. M., & McCarley, R. W. (2016) · Current Opinion in Psychiatry · doi:10.1097/yco.0000000000000244 · Cited by 144 · see citing works
Lewis, D. A. (2012) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.2012.08156.x · Cited by 142 · see citing works
Self-citationCortical basket cell dysfunction in schizophrenia
Curley, A. A., & Lewis, D. A. (2012) · The Journal of Physiology · doi:10.1113/jphysiol.2011.224659 · Cited by 136 · see citing works
“In a recent study (Curley et al. 2011), tissue sections were triple-labelled for GAD65, PV and GAD67.”
BackgroundInfluentialSelf-citationMolecular Mechanisms and Timing of Cortical Immune Activation in Schizophrenia
Volk, D. W., Chitrapu, A., Edelson, J. R., Roman, K. M., Moroco, A. E., & Lewis, D. A. (2015) · American Journal of Psychiatry · doi:10.1176/appi.ajp.2015.15010019 · Cited by 137 · see citing works
Self-citationGABA abnormalities in schizophrenia: A methodological review of in vivo studies
Taylor, S. F., & Tso, I. F. (2014) · Schizophrenia Research · doi:10.1016/j.schres.2014.10.011 · Cited by 125 · see citing works
“In schizophrenia, the most replicated findings are reductions in the 67-kDa isoform of the synthetic enzyme for GABA, glutamic acid decarboxylase (GAD67; Curley et al., 2011; Guidotti et al., 2000).”
Current findings and perspectives on aberrant neural oscillations in schizophrenia
Hirano, Y., & Uhlhaas, P. J. (2021) · Psychiatry and Clinical Neurosciences · doi:10.1111/pcn.13300 · Cited by 121 · see citing works
“Post-mortem data has consistently demonstrated that activity levels of GABAergic inhibitory PV-interneurons are decreased as evidenced by reductions in glutamic acid decarboxylase (GAD67), the major enzyme converting glutamate into GABA.(127) Lower GAD67 mRNA in PV interneurons(128) have been observed in hippocampus,(…”
BackgroundRenard, J., Szkudlarek, H. J., Kramar, C. P., Jobson, C. E. L., Moura, K., Rushlow, W. J., & Laviolette, S. R. (2017) · Scientific Reports · doi:10.1038/s41598-017-11645-8 · Cited by 125 · see citing works
Cholinergic connectivity: it's implications for psychiatric disorders
Scarr, E., Gibbons, A. S., Neo, J. H., Udawela, M., & Dean, B. (2013) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2013.00055 · Cited by 117 · see citing works
“, 2000, 2001), as is cortical GAD67 protein (Curley et al., 2011).”
The Role of Parvalbumin Interneurons in Neurotransmitter Balance and Neurological Disease
Nahar, L., Delacroix, B. M., & Nam, H. W. (2021) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2021.679960 · Cited by 118 · see citing works
“Pv-FSI inhibition of pyramidal neurons are reduced due to lower GAD67 mRNA expression and lower GAD67 protein, indicating less GABA synthesis (46, 76).”
BackgroundStedehouder, J., & Kushner, S. A. (2016) · Molecular Psychiatry · doi:10.1038/mp.2016.147 · Cited by 113 · see citing works
Cattane, N., Richetto, J., & Cattaneo, A. (2018) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2018.07.001 · Cited by 118 · see citing works
Hoftman, G. D., Datta, D., & Lewis, D. A. (2016) · Biological Psychiatry · doi:10.1016/j.biopsych.2016.05.022 · Cited by 109 · see citing works
Self-citationGilabert‐Juan, J., Varea, E., Guirado, R., Blasco‐Ibáñez, J. M., Crespo, C., & Nácher, J. (2012) · Neuroscience Letters · doi:10.1016/j.neulet.2012.09.032 · Cited by 109 · see citing works
Substantial DNA methylation differences between two major neuronal subtypes in human brain
Kozlenkov, A., Wang, M., Roussos, P., Rudchenko, S., Barbu, M., Bibikova, M. V., Klotzle, B., Dwork, A. J., Zhang, B., Hurd, Y. L., et al. (2015) · Nucleic Acids Research · doi:10.1093/nar/gkv1304 · Cited by 125 · see citing works
“Moreover, the dysfunction of inhibitory interneurons in the prefrontal cortex (PFC) is the one of the most consistent findings in the SCZ research (12–16).”
Identification of a Corticohabenular Circuit Regulating Socially Directed Behavior
Benekareddy, M., Stachniak, T. J., Bruns, A., Knoflach, F., von Kienlin, M., Künnecke, B., & Ghosh, A. (2017) · Biological Psychiatry · doi:10.1016/j.biopsych.2017.10.032 · Cited by 101 · see citing works
“The frontal cortex in patients with schizophrenia shows a marked gamma-aminobutyric acidergic deficit in postmortem studies (1).”
BackgroundInhibition of parvalbumin-expressing interneurons results in complex behavioral changes
Brown, J. A., Ramikie, T. S., Schmidt, M. J., Báldi, R., Garbett, K. A., Everheart, M., Warren, L. E., Gellért, L., Horváth, S., Patel, S., et al. (2015) · Molecular Psychiatry · doi:10.1038/mp.2014.192 · Cited by 103 · see citing works
Yanagi, M., Joho, R. H., Southcott, S. A., Shukla, A. A., Ghose, S., & Tamminga, C. A. (2014) · Molecular Psychiatry · doi:10.1038/mp.2013.49 · Cited by 102 · see citing works
Losing your inhibition: Linking cortical GABAergic interneurons to schizophrenia
Inan, M., Petros, T. J., & Anderson, S. A. (2012) · Neurobiology of Disease · doi:10.1016/j.nbd.2012.11.013 · Cited by 100 · see citing works
Tatard-Leitman, V. M., Jutzeler, C. R., Suh, J., Saunders, J. A., Billingslea, E. N., Morita, S., White, R. S., Featherstone, R. E., Ray, R., Ortinski, P. I., et al. (2014) · Biological Psychiatry · doi:10.1016/j.biopsych.2014.06.026 · Cited by 96 · see citing works
Prenatal stress and inhibitory neuron systems: implications for neuropsychiatric disorders
Fine, R., Zhang, J., & Stevens, H. E. (2014) · Molecular Psychiatry · doi:10.1038/mp.2014.35 · Cited by 96 · see citing works
Rowland, L. M., Summerfelt, A. T., Wijtenburg, S. A., Du, X. M., Chiappelli, J., Krishna, N., West, J., Muellerklein, F., Kochunov, P. V., & Hong, L. E. (2015) · JAMA Psychiatry · doi:10.1001/jamapsychiatry.2015.2680 · Cited by 96 · see citing works
Molecular substrates of schizophrenia: homeostatic signaling to connectivity
Landek‐Salgado, M. A., Faust, T. E., & Sawa, A. (2015) · Molecular Psychiatry · doi:10.1038/mp.2015.141 · Cited by 93 · see citing works
Marques, T. R., Ashok, A. H., Angelescu, I., Borgan, F., Myers, J., Lingford-Hughes, A. R., Nutt, D., Veronese, M., Turkheimer, F., & Howes, O. D. (2020) · Molecular Psychiatry · doi:10.1038/s41380-020-0711-y · Cited by 91 · see citing works
Kimoto, S., Bazmi, H. H., & Lewis, D. A. (2014) · American Journal of Psychiatry · doi:10.1176/appi.ajp.2014.14010004 · Cited by 91 · see citing works
“Furthermore, we replicated previous findings of lower GAD67 mRNA levels (9) in a new cohort of schizophrenia subjects.”
Self-citationDatta, D., Arion, D., Corradi, J., & Lewis, D. A. (2015) · Biological Psychiatry · doi:10.1016/j.biopsych.2015.03.030 · Cited by 92 · see citing works
Self-citationHarvey, L., & Boksa, P. (2011) · Neuropharmacology · doi:10.1016/j.neuropharm.2011.11.022 · Cited by 92 · see citing works
Schizophrenia as a Disorder of Molecular Pathways
Horváth, S., & Mirnics, K. (2014) · Biological Psychiatry · doi:10.1016/j.biopsych.2014.01.001 · Cited by 90 · see citing works
“For example, glutamate decarboxylase 1 (GAD1)/glutamate decarboxylase 67 (GAD67) underexpression appears to be a hallmark of the illness (25), and present in the majority of the subjects with the disease—yet, this cannot be explained by genetic susceptibility in the GAD1 gene itself— lifestyle, medication history, or…”
BackgroundDysregulated ErbB4 Splicing in Schizophrenia: Selective Effects on Parvalbumin Expression
Chung, D. W., Volk, D. W., Arion, D., Zhang, Y., Sampson, A. R., & Lewis, D. A. (2016) · American Journal of Psychiatry · doi:10.1176/appi.ajp.2015.15020150 · Cited by 86 · see citing works
“Consistent with these findings, protein levels of parvalbumin and GAD67 are also lower in parvalbumin axon terminals in schizophrenia (24, 25).”
Self-citationJiang, Z., Cowell, R. M., & Nakazawa, K. (2013) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2013.00116 · Cited by 89 · see citing works
“…mRNA reduction of PV (Hashimoto et al., 2003, 2008; Mellios et al., 2009; Fung et al., 2010; Volk et al., 2012), GAD67 (Hashimoto et al., 2003; Curley et al., 2011) or GAT1 (Volk et al., 2012) has been found in PVIs in the dorsolateral prefrontal cortex of individuals with schizophrenia.”
BackgroundEpigenetic mechanisms in schizophrenia
Akbarian, S. (2014) · Dialogues in Clinical Neuroscience · doi:10.31887/dcns.2014.16.3/sakbarian · Cited by 89 · see citing works
Perisomatic inhibition and cortical circuit dysfunction in schizophrenia
Lewis, D. A., Fish, K. N., Arion, D., & Gonzalez-Burgos, G. (2011) · Current Opinion in Neurobiology · doi:10.1016/j.conb.2011.05.013 · Cited by 87 · see citing works
Self-citationDienel, S. J., Schoonover, K. E., & Lewis, D. A. (2022) · Biological Psychiatry · doi:10.1016/j.biopsych.2022.03.002 · Cited by 81 · see citing works
Self-citationPaine, T. A., Swedlow, N., & Swetschinski, L. R. (2016) · Behavioural Brain Research · doi:10.1016/j.bbr.2016.10.012 · Cited by 84 · see citing works
Interneuronopathies and their role in early life epilepsies and neurodevelopmental disorders
Katsarou, A., Moshé, S. L., & Galanopoulou, A. S. (2017) · Epilepsia Open · doi:10.1002/epi4.12062 · Cited by 82 · see citing works
Animal models of gene–environment interaction in schizophrenia: A dimensional perspective
Ayhan, Y., McFarland, R., & Pletnikov, M. V. (2015) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2015.10.002 · Cited by 81 · see citing works
The role of glutamatergic inputs onto parvalbumin-positive interneurons: relevance for schizophrenia
Rotaru, D. C., Lewis, D. A., & González‐Burgos, G. (2012) · Reviews in the Neurosciences · doi:10.1515/revneuro-2011-0059 · Cited by 80 · see citing works
“…; Hanada et al. , 1987 ; Simpson et al. , 1989 ; Akbarian et al. , 1995 ; Benes et al. , 1996 ; Guidotti et al. , 2000 ; Mirnics et al. , 2000 ; Volk et al. , 2000 ; Hashimoto et al. , 2005, 2007, 2008 ; Straub et al. , 2007 ; Mellios et al. , 2009 ; Duncan et al. , 2010 ; Curley et al. , 2011 ).”
Self-citationNácher, J., Guirado, R., & Castillo-Gómez, E. (2013) · Neurochemical Research · doi:10.1007/s11064-013-0977-4 · Cited by 75 · see citing works
“These parallel changes of PSA-NCAM and GAD67 may reflect the already reported alterations of cortical inhibitory circuits in schizophrenia (for a review see [99]); in fact, a recent report has found that GAD67 mRNA and protein levels are significantly lower in the DLPFC of schizophrenic patients [111].”
ResultKathuria, A., Lopez-Lengowski, K., Watmuff, B., McPhie, D. L., Cohen, B. M., & Karmacharya, R. (2019) · Translational Psychiatry · doi:10.1038/s41398-019-0660-x · Cited by 73 · see citing works
Tao, R., Davis, K. N., Li, C., Shin, J. H., Gao, Y., Jaffe, A. E., Gondré‐Lewis, M. C., Weinberger, D. R., Kleinman, J. E., & Hyde, T. M. (2017) · Molecular Psychiatry · doi:10.1038/mp.2017.105 · Cited by 72 · see citing works
Nouel, D., Burt, M., Zhang, Y., Harvey, L., & Boksa, P. (2011) · European Neuropsychopharmacology · doi:10.1016/j.euroneuro.2011.08.001 · Cited by 70 · see citing works
The Role of Endocannabinoid Signaling in Cortical Inhibitory Neuron Dysfunction in Schizophrenia
Volk, D. W., & Lewis, D. A. (2015) · Biological Psychiatry · doi:10.1016/j.biopsych.2015.06.015 · Cited by 69 · see citing works
Self-citationHomeoprotein Signaling in the Developing and Adult Nervous System
Prochiantz, A., & Nardo, A. A. D. (2015) · Neuron · doi:10.1016/j.neuron.2015.01.019 · Cited by 67 · see citing works
Pietersen, C. Y., Mauney, S. A., Kim, S. S., Passeri, E., Lim, M. P., Rooney, R. J., Goldstein, J. M., Petryshen, T. L., Seidman, L. J., Shenton, M. E., et al. (2014) · Journal of Neurogenetics · doi:10.3109/01677063.2013.878339 · Cited by 67 · see citing works
CSF GABA is reduced in first-episode psychosis and associates to symptom severity
Orhan, F., Fatouros‐Bergman, H., Goiny, M., Malmqvist, A., Piehl, F., Červenka, S., Collste, K., Victorsson, P. I., Sellgren, C. M., Flyckt, L., et al. (2017) · Molecular Psychiatry · doi:10.1038/mp.2017.25 · Cited by 68 · see citing works
The Fragile Brain: Stress Vulnerability, Negative Affect and GABAergic Neurocircuits in Psychosis
Taylor, S. F., Grove, T. B., Ellingrod, V. L., & Tso, I. F. (2019) · Schizophrenia Bulletin · doi:10.1093/schbul/sbz046 · Cited by 67 · see citing works
Prefrontal Cortical GABA Modulation of Spatial Reference and Working Memory
Auger, M. L., & Floresco, S. (2014) · The International Journal of Neuropsychopharmacology · doi:10.1093/ijnp/pyu013 · Cited by 66 · see citing works
“mRNA and protein levels of the GABA synthesis enzyme glutamic acid decarboxylase-67 are consistently found to be reduced in the prefrontal cortex (PFC) of schizophrenics (Akbarian et al., 1995; Guidotti et al., 2000; Volk et al., 2000; Hashimoto et al., 2008; Thompson et al., 2009; Curley et al., 2011), potentially le…”
BackgroundMüller, I., Çalışkan, G., & Stork, O. (2014) · Genes Brain & Behavior · doi:10.1111/gbb.12188 · Cited by 65 · see citing works
Renard, J., Rushlow, W. J., & Laviolette, S. R. (2018) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2018.00281 · Cited by 62 · see citing works
“A reduction of GAD 67 mRNA and protein levels is observed in layers 1 through 5 of post-mortem dorsolateral PFC brain tissue from patients with schizophrenia (23, 24, 45, 58, 59).”
MethodGeorgiev, D., Arion, D., Enwright, J. F., Kikuchi, M., Minabe, Y., Corradi, J. P., Lewis, D. A., & Hashimoto, T. (2014) · American Journal of Psychiatry · doi:10.1176/appi.ajp.2013.13040468 · Cited by 61 · see citing works
“For example, in the prefrontal cortex of subjects with schizophrenia, parvalbumin neurons exhibit lower mRNA and protein levels of GAD67 (the 67-kDa isoform of glutamic acid decarboxylase, an enzyme for GABA synthesis) (5, 6), reduced immunoreactivity of GABA transporter 1 (a presynaptic GABA transporter) (7), and low…”
Self-citationMitchell, A., Jiang, Y., Peter, C. J., & Akbarian, S. (2014) · Schizophrenia Research · doi:10.1016/j.schres.2014.10.020 · Cited by 61 · see citing works
“It has been suggested that approximately one out of three disease cases are affected by a more robust, perhaps more than > 30% downregulation in expression when compared to unaffected controls (Curley et al., 2011; Volk et al., 2012).”
BackgroundChiu, P. W., Lui, S. S. Y., Hung, K. S. Y., Chan, R. C. K., Chan, Q., Sham, P. C., Cheung, E. F. C., & Mak, H. K. (2017) · Schizophrenia Research · doi:10.1016/j.schres.2017.07.021 · Cited by 60 · see citing works
Hui, K. K., Takashima, N., Watanabe, A., Chater, T. E., Matsukawa, H., Nekooki-Machida, Y., Nilsson, P., Endo, R., Goda, Y., Saido, T. C., et al. (2019) · Science Advances · doi:10.1126/sciadv.aau8237 · Cited by 59 · see citing works
“Postmortem studies using brain samples from ASD (6) and SZ (7) patients have revealed alterations in glutamic acid decarboxylase (GAD65 and GAD67) expression, further implicating defective GABAergic signaling in pathogenesis.”
BackgroundMarkedly Lower Glutamic Acid Decarboxylase 67 Protein Levels in a Subset of Boutons in Schizophrenia
Rocco, B. R., Lewis, D. A., & Fish, K. N. (2015) · Biological Psychiatry · doi:10.1016/j.biopsych.2015.07.022 · Cited by 58 · see citing works
“Although less wellstudied, the deficit in GAD67 mRNA has been reported to be accompanied by lower GAD67 protein levels (6, 7, 9).”
BackgroundResultInfluentialSelf-citationCortical GABA markers identify a molecular subtype of psychotic and bipolar disorders
Volk, D. W., Sampson, A. R., Zhang, Y. R., Edelson, J. R., & Lewis, D. A. (2016) · Psychological Medicine · doi:10.1017/s0033291716001446 · Cited by 58 · see citing works
“In addition, deficits in these GABA neuron-related mRNAs were not seen in all schizophrenia subjects relative to pair-matched unaffected comparison subjects (Curley et al. 2011; Volk et al. 2012).”
InfluentialSelf-citationPrenatal ontogeny as a susceptibility period for cortical GABA neuron disturbances in schizophrenia
Volk, D. W., & Lewis, D. A. (2013) · Neuroscience · doi:10.1016/j.neuroscience.2013.06.008 · Cited by 56 · see citing works
“…GABAsynthesizing enzyme GAD67 have been replicated across multiple subject cohorts and do not appear to be attributable to antipsychotic medications (Akbarian et al., 1995; Guidotti et al., 2000; Volk et al., 2000; Vawter et al., 2002; Straub et al., 2007; Duncan et al., 2010; Curley et al., 2011).”
BackgroundResultInfluentialSelf-citationTurkheimer, F., Leech, R., Expert, P., Lord, L.-D., & Vernon, A. C. (2015) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2015.04.014 · Cited by 54 · see citing works
White matter neuron biology and neuropathology in schizophrenia
Duchatel, R. J., Weickert, C. S., & Tooney, P. A. (2019) · Schizophrenia · doi:10.1038/s41537-019-0078-8 · Cited by 56 · see citing works
Synchrony in schizophrenia: a window into circuit-level pathophysiology
Spellman, T., & Gordon, J. A. (2014) · Current Opinion in Neurobiology · doi:10.1016/j.conb.2014.08.009 · Cited by 55 · see citing works
“Vierling-Claassen D, Siekmeier P, Stufflebeam S, Kopell N: Modeling GABA alterations in schizophrenia: a link between impaired inhibition and altered gamma and beta range auditory entrainment.”
InfluentialLanz, T. A., Joshi, J. J., Reinhart, V., Johnson, K., Grantham, L. E., & Volfson, D. (2015) · PLoS ONE · doi:10.1371/journal.pone.0121744 · Cited by 55 · see citing works
“Total RNA was prepared in a trizol-chloroform extraction from one set of sections, while protein was prepared in another set according to published methods [9].”
MethodGlausier, J. R., Kimoto, S., Fish, K. N., & Lewis, D. A. (2015) · Biological Psychiatry · doi:10.1016/j.biopsych.2014.05.010 · Cited by 53 · see citing works
Self-citationMapping pathologic circuitry in schizophrenia
Glausier, J. R., & Lewis, D. A. (2018) · Handbook of clinical neurology · doi:10.1016/b978-0-444-63639-3.00025-6 · Cited by 52 · see citing works
Self-citationNew Drug Treatments for Schizophrenia: A Review of Approaches to Target Circuit Dysfunction
Howes, O. D., Dawkins, E., Lobo, M. C., Kaar, S. J., & Beck, K. (2024) · Biological Psychiatry · doi:10.1016/j.biopsych.2024.05.014 · Cited by 52 · see citing works
Gilabert‐Juan, J., Bellés, M., Sáez-Ibáñez, A. R., Carceller, H., Zamarbide-Forés, S., Moltó, M. D., & Nácher, J. (2013) · Neurobiology of Disease · doi:10.1016/j.nbd.2013.07.008 · Cited by 53 · see citing works
“…GABA and some genes implicated in its metabolism have been associated with schizophrenia (Straub et al., 2007; Zai et al., 2009), specially the 67- kDa isoform of glutamic acid decarboxylase (GAD67) (see Akbarian and Huang, 2006; Beneyto and Lewis, 2011; Curley et al., 2011 for review).”
BackgroundTsubomoto, M., Kawabata, R., Zhu, X., Minabe, Y., Chen, K., Lewis, D. A., & Hashimoto, T. (2018) · Cerebral Cortex · doi:10.1093/cercor/bhy227 · Cited by 52 · see citing works
“First, in our previous analyses, none of comorbid factors, such as the presence of substance abuse/dependence at the time of death, the use of antidepressants, benzodiazepine/anticonvulsant or antipsychotics at the time of death, and suicide as the cause of death, had a significant effect on the expression of PV, SST,…”
BackgroundSelf-citationCurley, A. A., Eggan, S. M., Lazarus, M. S., Huang, Z. J., Volk, D. W., & Lewis, D. A. (2013) · Neurobiology of Disease · doi:10.1016/j.nbd.2012.10.018 · Cited by 51 · see citing works
“(Curley et al., 2011), suggesting that these mice appropriately recapitulate this aspect of the illness.”
BackgroundMethodResultInfluentialSelf-citationEarly-infantile onset epilepsy and developmental delay caused by bi-allelic GAD1 variants
Neuray, C., Maroofian, R., Scala, M., Sultan, T., Pai, G. S., Mojarrad, M., Khashab, H. Y. E., deHoll, L., Yue, W. W., Alsaif, H. S., et al. (2020) · Brain · doi:10.1093/brain/awaa178 · Cited by 51 · see citing works
“The severity of the Gad67 phenotype in animal models might suggest severe phenotypical manifestions in humans, yet there have been few reported families with GAD1 mutations (Lynex et al., 2004; Saito et al., 2010; Curley et al., 2011; Ruzicka et al., 2015; Magri et al., 2018).”
BackgroundAltered Markers of Cortical γ-Aminobutyric Acid Neuronal Activity in Schizophrenia
Kimoto, S., Zaki, M. M., Bazmi, H. H., & Lewis, D. A. (2015) · JAMA Psychiatry · doi:10.1001/jamapsychiatry.2015.0533 · Cited by 51 · see citing works
Self-citationCortical Opioid Markers in Schizophrenia and across Postnatal Development
Volk, D. W., Radchenkova, P., Er, W., Sengupta, E. J., & Lewis, D. A. (2011) · Cerebral Cortex · doi:10.1093/cercor/bhr202 · Cited by 51 · see citing works
Self-citationCannabis in Adolescence: Lasting Cognitive Alterations and Underlying Mechanisms
Scheyer, A. F., Laviolette, S. R., Pélissier‐Alicot, A., & Manzoni, O. J. (2022) · Cannabis and Cannabinoid Research · doi:10.1089/can.2022.0183 · Cited by 51 · see citing works
Neurobehavioral effects of long‐term maternal fructose intake in rat offspring
Erbaş, O., Erdoğan, M. A., Khalilnezhad, A., Gürkan, F. T., Yiğittürk, G., Meral, A., & Taşkıran, D. (2018) · International Journal of Developmental Neuroscience · doi:10.1016/j.ijdevneu.2018.07.001 · Cited by 49 · see citing works
“Decreased expression of GAD67 has been reported in the brain of individuals with schizophrenia (Curley et al., 2011) and autism (Fatemi et al., 2002).”
BackgroundSohal, V. S. (2022) · American Journal of Psychiatry · doi:10.1176/appi.ajp.20220147 · Cited by 48 · see citing works
Basta‐Kaim, A., Fijał, K., Ślusarczyk, J., Trojan, E., Głombik, K., Budziszewska, B., Leśkiewicz, M., Regulska, M., Kubera, M., Lasoń, W., et al. (2014) · Neuroscience · doi:10.1016/j.neuroscience.2014.12.013 · Cited by 48 · see citing works
Volk, D. W. (2016) · Neurobiology of Disease · doi:10.1016/j.nbd.2016.12.019 · Cited by 47 · see citing works
Self-citation
- Authors
- Curley, A. A., Arion, D., Volk, D. W., Asafu-Adjei, J. K., Sampson, A. R., Fish, K. N., & Lewis, D. A.
- Affiliations
- University of Pittsburgh (US)
- Venue
- American Journal of Psychiatry
- Published
- 2011-09
- Volume
- 168
- Issue
- 9
- Pages
- 921-929
- ISSN
- 0002-953X (ISSN-L)
- 1535-7228
- PMC
- PMC3273780
- OpenAlex
- W2159400463
- Cited by
- 283
- References
- 43
- Citations by year
- 2026: 10 · 2025: 13 · 2024: 11 · 2023: 15 · 2022: 13 · 2021: 16 · 2020: 12 · 2019: 22 · 2018: 24 · 2017: 20 · 2016: 23 · 2015: 28 · 2014: 28 · 2013: 23 · 2012: 16
- FWCI
- 16.41
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Bristol-Myers Squibb
- Pfizer
- AstraZeneca
- SK Life Science
- National Institutes of Health
- National Institute of Mental Health (P50MH084053, MH084053, R21MH085108, MH085108, R01MH043784, MH084016, K08MH084016, R37MH043784, MH043784)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- schizophrenia, glutamic acid decarboxylase 67, GAD67, GABA synthesis, dorsolateral prefrontal cortex, parvalbumin neurons, axon terminals, GABAergic interneurons, cognitive impairment, postmortem brain
- MeSH terms
- Adult, Cognition Disorders, Female, gamma-Aminobutyric Acid, Glutamate Decarboxylase, Humans, Male, Microscopy, Fluorescence, Middle Aged, Neurons, Parvalbumins, Reference Values, RNA, Messenger, Schizophrenia, Blotting, Western, Cohort Studies, Prefrontal Cortex, Presynaptic Terminals
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