The DOI matches its Crossref record.
Alternative excitotoxic hypotheses
Abstract
It is known that asthma is a heterogeneous entity whose manifestations vary with age. Our objective was to examine changes in the manifestation of asthma and asthma-related traits in childhood by defining empirically derived childhood asthma phenotypes and examining their transitions over time. To define the phenotypes we used data on respiratory symptoms, healthcare utilisation, medications, spirometry, airway hyperresponsiveness (AHR), exhaled nitric oxide concentration and atopy from a birth cohort recruited on the basis of having a first-degree relative with asthma. Data were acquired at ages 1.5–11.5 years and analysed using latent transition analysis. In a study population of 370 participants, we classified subjects into four phenotypes: 1) nonatopic, few symptoms (prevalence range from 1.5 to 5 years: 52–60%), 2) atopic, few symptoms (3–21%), 3) nonatopic, asthma and rhinitis symptoms (13–35%), and 4) atopic, asthma and rhinitis symptoms (2–14%) in early childhood; and 1) nonatopic, no respiratory disease (prevalence range from 8 to 11.5 years: 41–46%), 2) atopic, no respiratory disease (23–33%), 3) nonatopic, asthma symptoms, no AHR or airway inflammation (8–12%) and 4) atopic asthma (19%) in mid-childhood. Transitioning between phenotypes was common in early childhood, but less common in later childhood. This analysis represents the first attempt to incorporate longitudinal patterns of several manifestations of asthma into a single model to simultaneously define phenotypes and examine their transitions over time. It provides quantitative support for the view that asthma is a heterogeneous entity, and that some children with wheeze and other respiratory symptoms in early life progress to asthma in mid-childhood, while others become asymptomatic.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Damage to glutamatergic neurons, in particular cell bodies and neurites in layers III and IV of the neocortex, together with damage to glutamatergically-innervated cortical and hippocampal neurons, are particularly evident in AD brain (Albin and Greenamyre 1992).”
From Alzheimer’s disease: Targeting the glutamatergic system (2020) · cites this paper as Albin and Greenamyre 1992
Citations
Cited by
Sorted by citations
Items 101–200 of 573
Guyot, M., Hantraye, P., Dolan, R., Palfi, S., Mazière, M., & Brouillet, E. (1997) · Neuroscience · doi:10.1016/s0306-4522(96)00602-1 · Cited by 158
Schulz, J. B., Matthews, R. T., Henshaw, D. R., & Beal, M. F. (1996) · Neuroscience · doi:10.1016/0306-4522(95)00527-7 · Cited by 155
Mouse models of Huntington's disease and methodological considerations for therapeutic trials
Ferrante, R. J. (2009) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2009.04.001 · Cited by 157
Kim, S., Jeitner, T. M., & Steinert, P. M. (2002) · Neurochemistry International · doi:10.1016/s0197-0186(01)00064-x · Cited by 156
Taurine and central nervous system disorders
Menzie, J., Pan, C., Prentice, H. M., & Wu, J. (2012) · Amino Acids · doi:10.1007/s00726-012-1382-z · Cited by 153
“1 A simplified diagram, depicting the anatomical connections within the basal ganglia circuitry, according to the classical direct and indirect pathway model ''indirect excitotoxic hypothesis'' (Albin and Greenamyre 1992; Beal et al. 1993).”
MethodHow Mitochondrial Damage Affects Cell Function
James, A. M., & Murphy, M. P. (2002) · Journal of Biomedical Science · doi:10.1159/000064721 · Cited by 181
3-Nitropropionic acidʼs lethal triplet
Alexi, T., Hughes, P. E., Faull, R. L. M., & Williams, C. E. (1998) · Neuroreport · doi:10.1097/00001756-199808030-00001 · Cited by 149
Spatial relationship between synapse loss and β‐amyloid deposition in Tg2576 mice
Dong, H., Martin, M. V., Chambers, S., & Csernansky, J. G. (2006) · The Journal of Comparative Neurology · doi:10.1002/cne.21176 · Cited by 149
“The neurodegeneration observed in AD is mainly restricted to cell bodies and the dendrites of glutamatergic neurons in Layers III and IV of the neocortex (Albin and Greenamyre, 1992).”
BackgroundVion‐Dury, J., Meyerhoff, D. J., Cozzone, P. J., et al. (1994) · Journal of Neurology · doi:10.1007/bf02033352 · Cited by 145
“ping neuron damage, (3) evaluating membrane alterations, and (4) char-”
BackgroundInfluentialMcAdoo, D. J., Xu, G., Robak, G., & Hughes, M. G. (1999) · Experimental Neurology · doi:10.1006/exnr.1999.7166 · Cited by 142
Schwarz, M., Guillemin, G. J., Teipel, S. J., Büerger, K., & Hampel, H. J. (2012) · European Archives of Psychiatry and Clinical Neuroscience · doi:10.1007/s00406-012-0384-x · Cited by 141
“Additionally, AD leads to progressive loss of cortical and hippocampal neurons innervated by L-Glu [1].”
BackgroundThe Clinical and Genetic Features of Huntington Disease
Sturrock, A., & Leavitt, B. R. (2010) · Journal of Geriatric Psychiatry and Neurology · doi:10.1177/0891988710383573 · Cited by 144
Bradley, S. R., Marino, M. J., Wittmann, M., Rouse, S. T., Awad, H., Levey, A. I., & Conn, P. J. (2000) · The Journal of Neuroscience · doi:10.1523/jneurosci.20-09-03085.2000 · Cited by 141
“Furthermore, glutamate has been implicated as an excitotoxic agent in PD (Albin and Greenamyre, 1992; Rodriguez et al., 1998), suggesting that increased excitatory drive to the SNc may contribute to the progressive loss of SNc dopaminergic neurons in PD.”
BackgroundCell death and proliferation in acute slices and organotypic cultures of mammalian CNS
Lossi, L., Alasia, S., Salio, C., & Merighi, A. (2009) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2009.01.002 · Cited by 141
Exitatory Amino Acids in Health and Disease
THOMAS, R. J. (1995) · Journal of the American Geriatrics Society · doi:10.1111/j.1532-5415.1995.tb07407.x · Cited by 138
Ginés, S., Ivanova, E. V., Seong, I., Saura, C. A., & MacDonald, M. E. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m309348200 · Cited by 136
Stefani, A., Spadoni, F., & Bernardi, G. (1997) · Experimental Neurology · doi:10.1006/exnr.1997.6554 · Cited by 137
Kim, G. W., Gasche, Y., Grzeschik, S. M., Copin, J., Maier, C. M., & Chan, P. H. (2003) · Journal of Neuroscience · doi:10.1523/jneurosci.23-25-08733.2003 · Cited by 131
“The precise mechanism of this degeneration is unknown; however, oxidative stress and mitochondrial dysfunction-linked excitotoxicity have been proposed as key events in the pathophysiology of HD (Albin and Greenamyre, 1992; Coyle and Puttfarcken, 1993; Beal, 1995, 2000).”
Mechanistic Approaches to Parkinson's Disease Pathogenesis
Betarbet, R. S., Sherer, T., Monte, D. A. D., & Greenamyre, J. T. (2002) · Brain Pathology · doi:10.1111/j.1750-3639.2002.tb00468.x · Cited by 136
“Furthermore, complex I impairment may predispose neurons to excitotoxicity and oxidative damage, both of which have been implicated in the pathogenesis of PD (2, 34, 82).”
BackgroundSelf-citationCalabresi, P., Centonze, D., Pisani, A., Sancesario, G., Gubellini, P., Marfia, G. A., & Bernardi, G. (1998) · Annals of Neurology · doi:10.1002/ana.410430506 · Cited by 133
Li, X. J., Sharp, A. H., Li, S. H., Dawson, T. M., Snyder, S. H., & Ross, C. A. (1996) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.93.10.4839 · Cited by 133
Schwarzschild, M. A., Xu, K., Öztaş, E., Petzer, J. P., Castagnoli, K., Castagnoli, N. J., & Chen, J. (2003) · Neurology · doi:10.1212/01.wnl.0000095214.53646.72 · Cited by 130
Sapko, M. T., Guidetti, P., Yü, P., Tagle, D. A., Pellicciari, R., & Schwarcz, R. M. (2005) · Experimental Neurology · doi:10.1016/j.expneurol.2005.07.004 · Cited by 134
Wenk, G. L., Parsons, C. G., & Danysz, W. (2006) · Behavioural Pharmacology · doi:10.1097/00008877-200609000-00007 · Cited by 134
“Subsequent activation of NMDA receptors by glutamatergic synaptic activity may thus permit a continuous influx of calcium ions into neurons, theoretically overwhelming the endogenous mechanisms that regulate calcium ion homeostasis (Albin and Greenamyre, 1992; Chao and Hu, 1994).”
BackgroundJamwal, S., & Kumar, P. (2018) · Current Neuropharmacology · doi:10.2174/1570159x16666180302115032 · Cited by 130
Dopaminergic neurons degenerate by apoptosis in Parkinson's disease
Hirsch, É. C., Hunot, S., Faucheux, B. A., Agid, Y., Mizuno, Y., Mochizuki, H., Tatton, W. G., Tatton, N. A., & Olanow, W. C. (1999) · Movement Disorders · doi:10.1002/1531-8257(199903)14:2 · Cited by 152
In Vivo Calpain/Caspase Cross-talk during 3-Nitropropionic Acid-induced Striatal Degeneration
Bizat, N., Hermel, J., Humbert, S., Jacquard, C., Créminon, C., Escartin, C., Saudou, F., Krajewski, S., Hantraye, P., & Brouillet, E. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m305057200 · Cited by 125
Neuroinflammation Alters the Hippocampal Pattern of Behaviorally InducedArcExpression
Rosi, S., Ramı́rez-Amaya, V., Vazdarjanova, A. I., Worley, P. F., Barnes, C. A., & Wenk, G. L. (2005) · Journal of Neuroscience · doi:10.1523/jneurosci.4469-04.2005 · Cited by 124
“This scenario has become known as the " weak excitotoxicity " model (Albin and Greenamyre, 1992).”
BackgroundEnhanced astrocytic d-serine underlies synaptic damage after traumatic brain injury
Perez, E. J., Tapanes, S. A., Loris, Z. B., Balu, D. T., Sick, T. J., Coyle, J. T., & Liebl, D. J. (2017) · Journal of Clinical Investigation · doi:10.1172/jci92300 · Cited by 127
Zhang, H., Li, Q., Graham, R. K., Slow, E., Hayden, M. R., & Борисович, Б. И. (2008) · Neurobiology of Disease · doi:10.1016/j.nbd.2008.03.010 · Cited by 127
Gozal, D., Row, B. W., Kheirandish, L., Liu, R., Guo, S. Z., Fan, Q., & Brittian, K. R. (2003) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2003.01973.x · Cited by 123
Shehadeh, J., Fernandes, H. B., Mullins, M. Z., Graham, R. K., Leavitt, B. R., Hayden, M. R., & Raymond, L. A. (2005) · Neurobiology of Disease · doi:10.1016/j.nbd.2005.08.001 · Cited by 120
“A central hypothesis to explain selective neurodegeneration in HD is glutamatergic over-excitation and/or energetic failure at the level of the mitochondria (Albin and Greenamyre, 1992; Beal, 1992; Rego and Oliveira, 2003).”
BackgroundGoswami, A., Dikshit, P., Mishra, A., Mulherkar, S. A., Nukina, N., & Jana, N. R. (2006) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2006.01.136 · Cited by 124
“excitotoxicity [14].”
Glutamate receptor modulation by protein phosphorylation.
Raymond, L. A., Tingley, W., Blackstone, C., Roche, K. W., & Huganir, R. (1994) · Journal of Physiology - Paris · doi:10.1016/0928-4257(94)90004-3 · Cited by 124
Reactive oxygen species and the brain in sleep apnea
Wang, Y., Zhang, S. X. L., & Gozal, D. (2010) · Respiratory Physiology & Neurobiology · doi:10.1016/j.resp.2010.09.001 · Cited by 124
“This was consistent with the hypothesis that a chronic, slowly evolving glutamate excitotoxicity was one of the factors that underlie the structural and behavioral consequences of intermittent hypoxia in our model (Albin and Greenamyre, 1992).”
ResultSilva‐Adaya, D., Cruz, V. P. L., Herrera‐Mundo, M. N., Mendoza‐Macedo, K., Villeda‐Hernández, J., BINIENDA, Z. K., Ali, S. F., & Santamarı́a, A. (2007) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2007.05174.x · Cited by 119
“Indeed, it is accepted that these two mechanisms may be acting in a concerted (synergistic) manner, thus potentiating each other (Albin and Greenamyre 1992; Jacquard et al. 2006; Del Rio et al. 2007).”
BackgroundFontaine, M. A. L., Geddes, J. W., Banks, A., & Butterfield, D. A. (2000) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2000.0751709.x · Cited by 118
“Recently, the activation of excitatory amino acid receptors has been implicated in HD (Albin and Greenamyre, 1992; Beal, 1992).”
BackgroundVed, H. S., Koenig, M. L., Dave, J. R., & Doctor, B. P. (1997) · Neuroreport · doi:10.1097/00001756-199703030-00029 · Cited by 115
Alberch, J., Pérez‐Navarro, E., & Canals, J. M. (2002) · Brain Research Bulletin · doi:10.1016/s0361-9230(01)00775-4 · Cited by 116
Bernard, V., & Bolam, J. P. (1998) · European Journal of Neuroscience · doi:10.1046/j.1460-9568.1998.00380.x · Cited by 116
Role of excitotoxicity in human neurological disease
Beal, M. F. (1992) · Current Opinion in Neurobiology · doi:10.1016/0959-4388(92)90035-j · Cited by 114
Differential expression of N‐methyl‐d‐aspartate receptor NR2 isoforms in Alzheimer's disease
Hynd, M., Scott, H., & Dodd, P. R. (2004) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2004.02548.x · Cited by 118
Increased mitochondrial complex I activity in platelets of schizophrenic patients
Ben‐Shachar, D., Zuk, R., Gazawi, H., Reshef, A., Sheinkman, A., & Klein, E. (1999) · The International Journal of Neuropsychopharmacology · doi:10.1017/s1461145799001649 · Cited by 113
“Defects in mitochondrial function and the inability to maintain cellular ATP levels have been suggested to play a role in neurodegenerative diseases (Albin and Greenamyre, 1992 ; Beal, 1992) .”
Background(ANS), E. P. O. F. A. A. N. S. A. T. F., Mortensen, A., Aguilar, F., et al. (2017) · EFSA Journal · doi:10.2903/j.efsa.2017.4910 · Cited by 111
“These results supported the concept that over-stimulation of excitatory amino acid receptors could cause neuronal death (Schwarcz et al., 1984; Albin and Greenamyre, 1992).”
ResultGlutamate, excitotoxicity, and programmed cell death in parkinson disease
Caudle, W. M., & Zhang, J. (2009) · Experimental Neurology · doi:10.1016/j.expneurol.2009.09.027 · Cited by 107
“However, studies have suggested that the role of excitotoxicity in neurodegenerative diseases such as PD follows an indirect pathway (Albin and Greenamyre, 1992; Greene and Greenamyre, 1996).”
BackgroundOuary, S., Bizat, N., Altairac, S., Ménétrat, H., Mittoux, V., Condé, F., Hantraye, P., & Brouillet, E. (2000) · Neuroscience · doi:10.1016/s0306-4522(00)00020-8 · Cited by 111
Chapter 21 Glutamate toxicity in chronic neurodegenerative disease
Lancelot, E., & Beal, M. F. (1998) · Progress in brain research · doi:10.1016/s0079-6123(08)60446-x · Cited by 110
de Sousa, S. C., Maciel, E. N., Vercesi, A. E., & Castilho, R. F. (2003) · FEBS Letters · doi:10.1016/s0014-5793(03)00421-6 · Cited by 109
Abnormal calcium homeostasis and mitochondrial polarization in a human encephalomyopathy.
Moudy, A. M., Handran, S. D., Goldberg, M. P., Ruffin, N., Karl, I. E., Kranz‐Eble, P., DeVivo, D. C., & Rothman, S. M. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.3.729 · Cited by 109
Braidy, N., Grant, R., Adams, S., & Guillemin, G. J. (2009) · FEBS Journal · doi:10.1111/j.1742-4658.2009.07487.x · Cited by 110
Transmembrane topology of the glutamate receptor subunit GluR6.
Roche, K. W., Raymond, L. A., Blackstone, C. D., & Huganir, R. L. (1994) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(17)32623-6 · Cited by 108
Gozal, E., Gozal, D., Pierce, W. M. J., Thongboonkerd, V., Scherzer, J. A., Sachleben, L. R., Brittian, K. R., Guo, S., Cai, J., & Klein, J. B. (2002) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2002.01134.x · Cited by 107
Kumar‐Singh, S., Dewachter, I., Moechars, D., Lübke, U., Jonghe, C. D., Ceuterick, C., Checler, F., Naidu, A., Cordell, B., Cras, P. P., et al. (2000) · Neurobiology of Disease · doi:10.1006/nbdi.1999.0272 · Cited by 106
Assessment of coenzyme q10 tolerability in huntington's disease
Feigin, A., Kieburtz, K. D., Como, P. G., Hickey, C., Abwender, D. A., Zimmerman, C., Steinberg, K., & Shoulson, I. (1996) · Movement Disorders · doi:10.1002/mds.870110317 · Cited by 108
K�ppenbender, K. D., Standaert, D. G., Feuerstein, T. J., Penney, J. B., Young, A. B., & Landwehrmeyer, G. B. (2000) · The Journal of Comparative Neurology · doi:10.1002/(sici)1096-9861(20000417)419:4 · Cited by 104
Hypoxia and related conditions
Auer, R. N., Dunn, J. F., & Sutherland, G. R. (2008) · CRC Press eBooks · doi:10.1201/b13319-3 · Cited by 104
CONNEXIN EXPRESSION IN HUNTINGTON'S DISEASED HUMAN BRAIN
Vis, J. C., Nicholson, L. F. B., Faull, R. L. M., Evans, W. H., Severs, N. J., & Green, C. R. (1998) · Cell Biology International · doi:10.1006/cbir.1998.0388 · Cited by 102
Figueredo-Cardenas, G., Harris, C. L., Anderson, K. D., & Reiner, A. J. (1998) · Experimental Neurology · doi:10.1006/exnr.1997.6724 · Cited by 100
Huntington Disease and the Related Disorder, Dentatorubral-Pallidoluysian Atrophy (DRPLA)
Ross, C. A., Margolis, R. L., Rosenblatt, A., Ranen, N. G., Bêcher, M. W., & Aylward, E. (1997) · Medicine · doi:10.1097/00005792-199709000-00001 · Cited by 101
Patel, S., Hamill, T. G., Connolly, B., Jagoda, E. M., Li, W., & Gibson, R. E. (2007) · Nuclear Medicine and Biology · doi:10.1016/j.nucmedbio.2007.07.009 · Cited by 100
MacDonald, M. E., Ginés, S., Gusella, J. F., & Wheeler, V. C. (2003) · NeuroMolecular Medicine · doi:10.1385/nmm:4:1-2:7 · Cited by 104
“The subsequent molecular changes implicate excitotoxicity, which has been hypothesized to play a central role in neurodegeneration (Albin and Greenamyre, 1992).”
BackgroundPetersén, Å., Castilho, R. F., Hansson, O., Wieloch, T. W., & Brundin, P. (2000) · Brain Research · doi:10.1016/s0006-8993(99)02320-3 · Cited by 99
Excitatory Amino Acids in Cerebrospinal Fluid of Patients with Acute Head Injuries
Zhang, H., Xinding, Z., Tianlin, Z., et al. (2001) · Clinical Chemistry · doi:10.1093/clinchem/47.8.1458 · Cited by 98
Lactic acidosis and other mitochondrial disorders
Stacpoole, P. W. (1997) · Metabolism · doi:10.1016/s0026-0495(97)90259-6 · Cited by 98
Glutamate Receptors and Parkinson???s Disease
Marino, M. J., Valenti, O., & Conn, P. J. (2003) · Drugs & Aging · doi:10.2165/00002512-200320050-00006 · Cited by 97
Huntington's disease: translating a CAG repeat into a pathogenic mechanism
MacDonald, M. E., & Gusella, J. F. (1996) · Current Opinion in Neurobiology · doi:10.1016/s0959-4388(96)80097-3 · Cited by 96
James, A. M., Sheard, P. W., Wei, Y., & Murphy, M. P. (1999) · European Journal of Biochemistry · doi:10.1046/j.1432-1327.1999.00066.x · Cited by 93
Valenti, O., Mannaioni, G., Seabrook, G. R., Conn, P. J., & Marino, M. J. (2005) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.104.080481 · Cited by 92
“In addition, an indirect excitotoxic hypothesis has been proposed to explain, in part, the degeneration of dopamine neurons in PD (Albin and Greenamyre, 1992).”
BackgroundRigby, M., Bourdellès, B. L., HEAVENS, R. P., Kelly, S., Smith, D. W., Butler, A., Hammans, R., Hills, R., Xuereb, J. H., Hill, R., et al. (1996) · Neuroscience · doi:10.1016/0306-4522(96)00089-9 · Cited by 93
Glutamatergic Influences on the Basal Ganglia
Greenamyre, J. T. (2001) · Clinical Neuropharmacology · doi:10.1097/00002826-200103000-00001 · Cited by 90
Self-citationHIV‐1‐induced neuronal injury in the developing brain
Epstein, L. G., & Gelbard, H. (1999) · Journal of Leukocyte Biology · doi:10.1002/jlb.65.4.453 · Cited by 100
Intermittent Hypoxia and Cognitive Function: Implications from Chronic Animal Models
Row, B. W. (2007) · Advances in experimental medicine and biology · doi:10.1007/978-0-387-75434-5_5 · Cited by 90
Mitochondrial Inhibition and Oxidative Stress: Reciprocating Players in Neurodegeneration
Zeevalk, G. D., Bernard, L. P., Song, C., Gluck, M. J., & Ehrhart, J. (2005) · Antioxidants and Redox Signaling · doi:10.1089/ars.2005.7.1117 · Cited by 89
“…excitotoxic hypothesis predicts that a partial reduction in energy stores (ATP/ADP), compromised Na + ,K + -ATPase activity, and a deteriorating membrane potential may contribute to loss of regulation at the NMDA receptor via loss of the voltage-sensitive Mg 2+ - channel blockade (5, 95, 108, 264).”
Fain, J. N. (2001) · Human Molecular Genetics · doi:10.1093/hmg/10.2.145 · Cited by 87
Turski, L., & Turski, W. A. (1993) · Cellular and Molecular Life Sciences · doi:10.1007/bf01929915 · Cited by 88
Kölker, S., Schwab, M. A., Hörster, F., et al. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m308861200 · Cited by 87
Michael, L. G. (1999) · Frontiers in bioscience · doi:10.2741/garcia · Cited by 87
“This glutamate excitotoxicity is thought to be the final common pathway of acute injuries such as seizures or hypoxia, as well as of many neurodegenerative diseases such as Alzheimer and Huntington’s disease (76-80).”
Maciel, E. N., Kowaltowski, A. J., Schwalm, F. D., Rodrigues, J. M., Souza, D. O., Vercesi, A. E., Wajner, M., & Castilho, R. F. (2004) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2004.02565.x · Cited by 82
Wenk, G. L., McGann-Gramling, K. R., Hauss‐Wegrzyniak, B., Ronchetti, D., Maucci, R., Rosi, S., Gasparini, L., & Ongini, E. (2004) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2004.02359.x · Cited by 85
Chronic brain inflammation leads to a decline in hippocampal NMDA-R1 receptors.
Rosi, S., Ramı́rez-Amaya, V., Hauss‐Wegrzyniak, B., et al. (2004) · Journal of Neuroinflammation · doi:10.1186/1742-2094-1-12 · Cited by 85
Araujo, D. M., & Hilt, D. C. (1997) · Neuroscience · doi:10.1016/s0306-4522(97)00079-1 · Cited by 85
Cellular localization of pan-trk immunoreactivity and trkC mRNA in the enteric nervous system
Sternini, C., Su, D. K. M., Arakawa, J., GIORGIO, R. D., Rickman, D. W., Davis, B. M., Albers, K. M., & Brecha, N. C. (1996) · The Journal of Comparative Neurology · doi:10.1002/(sici)1096-9861(19960513)368:4 · Cited by 35
Gratacòs, E., Pérez‐Navarro, E., Tolosa, E. S., Arenas, E., & Alberch, J. (2001) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2001.00538.x · Cited by 84
“…death, is responsible for many neurological disorders ranging from acute insults, such as stroke, hypoglycemia and epilepsy, to chronic neurodegenerative diseases, such as Huntington's disease or amyotrophic lateral sclerosis (for a review see Albin and Greenamyre 1992; Lipton and Rosenberg 1994).”
BackgroundKordower, J., Isacson, O., & Emerich, D. (1999) · Experimental Neurology · doi:10.1006/exnr.1999.7156 · Cited by 91
Jara, J. H., Singh, B. B., Floden, A. M., & Combs, C. K. (2006) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2006.04330.x · Cited by 84
Creatine reduces 3-nitropropionic-acid-induced cognitive and motor abnormalities in rats
Shear, D. A., Haik, K. L., & Dunbar, G. L. (2000) · Neuroreport · doi:10.1097/00001756-200006260-00007 · Cited by 82
Emerich, D. F., Cain, C. K., Greco, C., Saydoff, J. A., Hu, Z. Y., Liu, H., & Lindner, M. D. (1997) · Cell Transplantation · doi:10.1016/s0963-6897(97)00035-3 · Cited by 91
Neuroprotective Effects of Synaptic Modulation in Huntington's Disease R6/2 Mice
Stack, E. C., Dedeoglu, A., Smith, K. M., Cormier, K., Kubilus, J. K., Bogdanov, M. B., Matson, W. R., Yang, L., Jenkins, B. G., Luthi‐Carter, R., et al. (2007) · Journal of Neuroscience · doi:10.1523/jneurosci.4318-07.2007 · Cited by 80
“The latter contributes to cell death in HD by causing increased vulnerability to endogenous concentrations of glutamate, which then results in excitotoxic cell death (Albin and Greenamyre, 1992; Beal, 1992; Ferrante et al., 1993).”
BackgroundVulnerability of Medium Spiny Striatal Neurons to Glutamate: Role of Na+/K+ ATPase
Calabresi, P., Murtas, M. D., Pisani, A., et al. (1995) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.1995.tb00689.x · Cited by 80
Yasuda, R. P., Ikonomovic, M. D., Sheffield, R., Rubin, R. T., Wolfe, B. B., & Armstrong, D. M. (1995) · Brain Research · doi:10.1016/0006-8993(95)00178-s · Cited by 71
Cui, X., Bao, L., Wang, X., & Chen, C. (2020) · Small · doi:10.1002/smll.201907665 · Cited by 80
Greene, J. G., Sheu, S. S., Gross, R. A., & Greenamyre, J. T. (1998) · Neuroscience · doi:10.1016/s0306-4522(97)00389-8 · Cited by 79
Self-citationCicchetti, F., & Parent, A. (1996) · Movement Disorders · doi:10.1002/mds.870110605 · Cited by 76
Neuropathology and pathogenesis of mitochondrial diseases
Brown, G. K., & Squier, M. V. (1996) · Journal of Inherited Metabolic Disease · doi:10.1007/bf01799116 · Cited by 77
Chemical preconditioning: A cytoprotective strategy
Riepe, M. W., & Ludolph, A. C. (1997) · Springer eBooks · doi:10.1007/978-1-4615-6111-8_39 · Cited by 75
Neuroprotective activity of acetyl‐L‐carnitine: Studies in vitro
Forloni, G., Angeretti, N., & Smiroldo, S. (1994) · Journal of Neuroscience Research · doi:10.1002/jnr.490370112 · Cited by 73
Nasr, P., Gursahani, H., Pang, Z., Bondada, V., Lee, J., Hadley, R. W., & Geddes, J. W. (2003) · Neurochemistry International · doi:10.1016/s0197-0186(02)00229-2 · Cited by 76
Neuroprotective effects of creatine administration against NMDA and malonate toxicity
Malcon, C., Kaddurah-Daouk, R. F., & Beal, M. F. (2000) · Brain Research · doi:10.1016/s0006-8993(00)02038-2 · Cited by 76
Duty, S. (2012) · CNS Drugs · doi:10.1007/s40263-012-0016-z · Cited by 75
Acetate supplementation attenuates lipopolysaccharide‐induced neuroinflammation
Reisenauer, C. J., Bhatt, D. P., Mitteness, D. J., Slanczka, E. R., Gienger, H. M., Watt, J. A., & Rosenberger, T. A. (2011) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2011.07198.x · Cited by 73
Metadata
- Authors
- Albin, R. L., & Greenamyre, J. T.
- Affiliations
- University of Michigan (US)
- University of Rochester (US)
- Venue
- Neurology
- Published
- 1992-04
- Volume
- 42
- Issue
- 4
- Pages
- 733-733
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- OpenAlex
- W2058176457
- Cited by
- 574
- References
- 0
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 6 · 2023: 3 · 2022: 18 · 2021: 4 · 2020: 12 · 2019: 3 · 2018: 6 · 2017: 7 · 2016: 5 · 2015: 4 · 2014: 10 · 2013: 12 · 2012: 16
- FWCI
- 14.01
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5k08ns001300-03, 5k08ns001487-03)
- National Institute of Neurological Disorders and Stroke (NS01300, NS 01487)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Asthma and respiratory diseases
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Occupational exposure and asthma
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Respiratory and Cough-Related Research
- Keywords
- asthma phenotypes, childhood asthma, asthma heterogeneity, phenotype transition, atopy, rhinitis, airway hyperresponsiveness, exhaled nitric oxide, wheezing, latent transition analysis, birth cohort
- MeSH terms
- Acute Disease, Amino Acids, Chronic Disease, Humans, Models, Neurological, Nerve Degeneration, Nervous System Diseases, Neurology, Neurotoxins, Receptors, Cell Surface, Receptors, Amino Acid
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review