Cited by 574Asthma and respiratory diseasesOccupational exposure and asthmaRespiratory and Cough-Related Research

The DOI matches its Crossref record.

Alternative excitotoxic hypotheses

Albin, Roger L., Greenamyre, J. Timothy·1992·Neurology

Open this paper in CoChat — free account

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.

Integrity signals

Registry

Crossref · 10.1212/wnl.42.4.733

Cites

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

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?

Sorted by citations

Items 201–300 of 573

Suppressive effect of Yokukansan on excessive release of glutamate and aspartate in the hippocampus of zinc-deficient rats
Takeda, A., Itoh, H., Tamano, H., Yuzurihara, M., & Oku, N. (2008) · Nutritional Neuroscience · doi:10.1179/147683008x301414 · Cited by 74
Neurotransmission systems in Parkinson’s disease
Moghaddam, H. S., Zare-Shahabadi, A., Rahmani, F., & Rezaei, N. (2017) · Reviews in the Neurosciences · doi:10.1515/revneuro-2016-0068 · Cited by 78
Apelin, a promising target for Alzheimer disease prevention and treatment
Masoumi, J., Abbasloui, M., Parvan, R., Mohammadnejad, D., Pavon‐Djavid, G., Barzegari, A., & Abdolalizadeh, J. (2018) · Neuropeptides · doi:10.1016/j.npep.2018.05.008 · Cited by 70
Dapagliflozin improves behavioral dysfunction of Huntington's disease in rats via inhibiting apoptosis-related glycolysis
El-Sahar, A. E., Rastanawi, A. A., El-Yamany, M. F., & Saad, M. A. (2020) · Life Sciences · doi:10.1016/j.lfs.2020.118076 · Cited by 71
The therapeutic role of creatine in Huntington's disease
Ryu, H., Rosas, H. D., Hersch, S. M., & Ferrante, R. J. (2005) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2005.04.008 · Cited by 69
Brainstem Activation of Platelet‐Derived Growth Factor‐β Receptor Modulates the Late Phase of the Hypoxic Ventilatory Response
Gozal, D., Simakajornboon, N., Czapla, M. A., Xue, Y., Gozal, E., Vlašić, V., Lasky, J. A., & Liu, J. (2000) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2000.0740310.x · Cited by 70
Brain-derived neurotrophic factor prevents the loss of nigral neurons induced by excitotoxic striatal-pallidal lesions
Volpe, B. T., Wildmann, J., & Altar, C. A. (1998) · Neuroscience · doi:10.1016/s0306-4522(97)00424-7 · Cited by 70
Metabolic Compromise with Systemic 3-Nitropropionic Acid Produces Striatal Apoptosis in Sprague–Dawley Rats but Not in BALB/c ByJ Mice
Alexi, T., Hughes, P. E., Knüsel, B., & Tobin, A. J. (1998) · Experimental Neurology · doi:10.1006/exnr.1998.6842 · Cited by 70
Mitochondrial energy metabolism in neurodegeneration associated with methylmalonic acidemia
de Melo, D. R., Kowaltowski, A. J., Wajner, M., et al. (2011) · Journal of Bioenergetics and Biomembranes · doi:10.1007/s10863-011-9330-2 · Cited by 69
Protective effects of ginseng components in a rodent model of neurodegeneration
Lian, X., Zhang, Z., & Stringer, J. L. (2005) · Annals of Neurology · doi:10.1002/ana.20450 · Cited by 69
Mitochondrial toxins and neurodegenerative diseases
Ayala, A. (2006) · Frontiers in bioscience · doi:10.2741/2119 · Cited by 68
“These changes are strikingly similar to those described in HD striatum (168-170).”
Method
The paradigm of Huntington’s disease: Therapeutic opportunities in neurodegeneration
Leegwater‐Kim, J., & Cha, J.-H. J. (2004) · NeuroRx · doi:10.1602/neurorx.1.1.128 · Cited by 68
Pathological Consequences of Intermittent Hypoxia in the Central Nervous System
Zhang, S. X. L., Wang, Y., & Gozal, D. (2012) · Comprehensive physiology · doi:10.1002/cphy.c100060 · Cited by 74
“…with reductions in the density of NMDA R1 receptor-expressing cells in the CA1 ﬁeld of hippocampus (44), and reductions in NMDA receptor-binding sites (117), suggesting the involvement of excitotoxic processes that may underlie the unique vulnerability of NMDA R1-expressing cells to IH (1,44).”
Effects of Ceftriaxone on the Behavioral and Neuronal Changes in an MPTP-Induced Parkinson’s Disease Rat Model
Ho, S.-C., Hsu, C.-C., Pawlak, C. R., Tikhonova, M. A., Lai, T.-J., Amstislavskaya, T. G., & Ho, Y.-J. (2014) · Behavioural Brain Research · doi:10.1016/j.bbr.2014.04.022 · Cited by 65
Effects of maternal oral administration of monosodium glutamate at a late stage of pregnancy on developing mouse fetal brain
Yu, T., Zhao, Y., Shi, W., Ma, R., & Yu, L. (1997) · Brain Research · doi:10.1016/s0006-8993(96)01181-x · Cited by 66
Functional characterization of CP-465,022, a selective, noncompetitive AMPA receptor antagonist
Lazzaro, J. T., Paternain, A. V., Lerma, J., Chenard, B. L., Ewing, F. E., HUANG, J., WELCH, W. M., Ganong, A. H., & Menniti, F. S. (2002) · Neuropharmacology · doi:10.1016/s0028-3908(01)00170-8 · Cited by 66
Neurotoxic effects of silver nanoparticles and the protective role of rutin
Ahmed, M. M., & Hussein, M. (2017) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2017.04.026 · Cited by 67
Huntington's disease, energy, and excitotoxicity
Beal, M. F. (1994) · Neurobiology of Aging · doi:10.1016/0197-4580(94)90132-5 · Cited by 67
Spatial and temporal expression of short, long/medium or both opsins in human fetal cones
Xiao (2000) · doi:10.1002/1096-9861(20001002)425:4
GlutamateNMDA receptor NR1 subunit mRNA expression in Alzheimer's disease
Hynd, M. R., Scott, H. L., & Dodd, P. R. (2001) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2001.00409.x · Cited by 66
Blockade of metabotropic glutamate receptors inhibits cognition and neurodegeneration in an MPTP-induced Parkinson's disease rat model
Hsieh, M., Ho, S.-C., Yeh, K.-Y., Pawlak, C. R., Chang, H., Ho, Y., Lai, T.-J., & Wu, F.-Y. (2012) · Pharmacology Biochemistry and Behavior · doi:10.1016/j.pbb.2012.03.022 · Cited by 65
Therapeutic horizons for amyotrophic lateral sclerosis
Rothstein, J. D. (1996) · Current Opinion in Neurobiology · doi:10.1016/s0959-4388(96)80103-6 · Cited by 65
β-Amyloid produces a delayed NMDA receptor- dependent reduction in synaptic transmission in rat hippocampus
Cullen, W. K., Wu, J., Anwyl, R., & Rowan, M. J. (1996) · Neuroreport · doi:10.1097/00001756-199612200-00018 · Cited by 65
Group I Metabotropic Glutamate Receptors Mediate an Inward Current in Rat Substantia Nigra Dopamine Neurons That Is Independent From Calcium Mobilization
Guatteo, E., Mercuri, N. B., Bernardi, G., et al. (1999) · Journal of Neurophysiology · doi:10.1152/jn.1999.82.4.1974 · Cited by 65
“In a pathological context a dysfunction of the mGluR1mediated inward current might alter the activity of the dopaminergic system in psychiatric disorders and participate to the excitotoxic neurodegeneration underlying Parkinson’s disease (Albin and Greenamyre 1992;Carlsson and Carlsson 1990).”
Background
Brain mitochondrial defects amplify intracellular [Ca2+] rise and neurodegeneration but not Ca2+entry during NMDA receptor activation
Jacquard, C., Trioulier, Y., Cosker, F., Escartin, C., Bizat, N., Hantraye, P., Cancela, J., Bonvento, G., & Brouillet, E. (2006) · The FASEB Journal · doi:10.1096/fj.05-5085fje · Cited by 66
New insights into progressive supranuclear palsy
Albers, D. S., & Augood, S. J. (2001) · Trends in Neurosciences · doi:10.1016/s0166-2236(00)01794-x · Cited by 62
Huntington's Disease and Dentatorubral‐Pallidoluysian Atrophy: Proteins, Pathogenesis and Pathology
Ross, C. A., Bêcher, M. W., Colomer, V., Engelender, S., Wood, J. D., & Sham, A. H. (1997) · Brain Pathology · doi:10.1111/j.1750-3639.1997.tb00898.x · Cited by 63
Ceftriaxone Prevents and Reverses Behavioral and Neuronal Deficits in an MPTP-Induced Animal Model of Parkinson’s Disease Dementia
Hsu, C.-Y., Hung, C.-S., Chang, H.-M., Liao, W.-C., Ho, S.-C., & Ho, Y.-J. (2015) · Neuropharmacology · doi:10.1016/j.neuropharm.2014.11.023 · Cited by 63
Subthalamic infusion of an NMDA antagonist prevents basal ganglia metabolic changes and nigral degeneration in a rodent model of Parkinson's disease
Blandini, F., Nappi, G., & Greenamyre, J. T. (2001) · Annals of Neurology · doi:10.1002/ana.104 · Cited by 62
Self-citation
The endogenous cofactors, thioctic acid and dihydrolipoic acid, are neuroprotective against NMDA and malonic acid lesions of striatum
Greenamyre, J. T., Garcia‐Osuna, M., & Greene, J. G. (1994) · Neuroscience Letters · doi:10.1016/0304-3940(94)90593-2 · Cited by 62
Self-citation
Subthalamic Ablation Reverses Changes in Basal Ganglia Oxidative Metabolism and Motor Response to Apomorphine Induced by Nigrostriatal Lesion in Rats
Blandini, F., Garcia‐Osuna, M., & Greenamyre, J. T. (1997) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.1997.tb01495.x · Cited by 61
Self-citation
Chemical preconditioning: A cytoprotective strategy
Riepe, M. W., & Ludolph, A. C. (1997) · Molecular and Cellular Biochemistry · doi:10.1023/a:1006820927262 · Cited by 61
6-Hydroxydopamine Injections into the Nigrostriatal Pathway Attenuate Striatal Malonate and 3-Nitropropionic Acid Lesions
Maragos, W. F., Jakel, R. J., Pang, Z., & Geddes, J. W. (1998) · Experimental Neurology · doi:10.1006/exnr.1998.6918 · Cited by 61
Ca2+ and Na+ Dependence of 3-Hydroxyglutarate-Induced Excitotoxicity in Primary Neuronal Cultures from Chick Embryo Telencephalons
Kölker, S., Köhr, G., Ahlemeyer, B., Okun, J. G., Pawlak, V., Hörster, F., Mayatepek, E., Krieglstein, J., & Hoffmann, G. F. (2002) · Pediatric Research · doi:10.1203/00006450-200208000-00011 · Cited by 60
“Apart from this, primary inhibition of mitochondrial respiratory chain activity has been shown to indirectly induce NMDA receptor stimulation and excitotoxic damage, and therefore has been termed “secondary” excitotoxicity (15, 16).”
Background
The use of transgenic and knock-in mice to study Huntington’s disease
Hickey, M. A., & Chesselet, M.-F. (2003) · Cytogenetic and Genome Research · doi:10.1159/000072863 · Cited by 61
“This was later found to be more successful as an explanation for acute brain damage (Albin and Greenamyre, 1992; Greene and Greenamyre, 1996).”
Background
Genetic polymorphisms in methylenetetrahydrofolate reductase and methionine synthase, folate levels in red blood cells, and risk of neural tube defects
Christensen, B., Arbour, L. T., Tran, P. V., Leclerc, D., Sabbaghian, N., Platt, R. W., Gilfix, B. M., Rosenblatt, D. S., Gravel, R. A., Forbes, P. A., et al. (1999) · American Journal of Medical Genetics · doi:10.1002/(sici)1096-8628(19990521)84:2 · Cited by 305
Involvement of Superoxide in Excitotoxicity and DNA Fragmentation in Striatal Vulnerability in Mice after Treatment with the Mitochondrial Toxin, 3-Nitropropionic Acid
Kim, G. W., & Chan, P. H. (2002) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1097/00004647-200207000-00005 · Cited by 59
“Mitochondrial dysfunction, excitotoxicity, and oxidative stress are interacting processes in the pathogenesis of neurodegenerative diseases such as Huntington’s disease (HD), Parkinson’s disease, amyotrophic lateral sclerosis, and Alzheimer’s disease (Albin and Greenamyre, 1992; Beal, 1992, 2000).”
Background
Interference with cellular energy metabolism reduces kynurenic acid formation in rat brain slices: reversal by lactate and pyruvate
Hodgkins, P., & Schwarcz, R. M. (1998) · European Journal of Neuroscience · doi:10.1046/j.1460-9568.1998.00208.x · Cited by 59
“Acute or chronic excitotoxic mechanisms, coupled to failure of cerebral energy metabolism, are likely to play a part in neurodegenerative diseases (Albin & Greenamyre, 1992; Beal, 1992; cf. also Peuchenet al., 1997).”
Background
DAMAGE AND REPAIR OF NERVE CELL DNA IN TOXIC STRESS*
Kisby, G. E., KABEL, H., Hugon, J., & Spencer, P. S. (1999) · Drug Metabolism Reviews · doi:10.1081/dmr-100101937 · Cited by 58
Apoptosis, Neurotrophic Factors and Neurodegeneration
Dragunow, M., MacGibbon, G. A., Lawlor, P. A., Butterworth, N. J., Connor, B. J., Henderson, C. E., Walton, M. R., Woodgate, A.-M., Hughes, P. E., & Faull, R. L. M. (1997) · Reviews in the Neurosciences · doi:10.1515/revneuro.1997.8.3-4.223 · Cited by 58
MPP+Produces Progressive Neuronal Degeneration Which Is Mediated by Oxidative Stress
Fallon, J., Matthews, R. T., Hyman, B. T., & Beal, M. F. (1997) · Experimental Neurology · doi:10.1006/exnr.1997.6416 · Cited by 57
Probucol modulates oxidative stress and excitotoxicity in Huntington's disease models in vitro
Colle, D., Hartwig, J. M., Soares, F. A. A., & Farina, M. (2012) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2012.01.003 · Cited by 61
Ischemic Injury to White Matter: An Age-Dependent Process
Baltan, S. (2009) · The Neuroscientist · doi:10.1177/1073858408324788 · Cited by 57
Differential inhibitory effects of methylmalonic acid on respiratory chain complex activities in rat tissues
Pettenuzzo, L. F., Ferreira, G. C., Schmidt, A. L., et al. (2005) · International Journal of Developmental Neuroscience · doi:10.1016/j.ijdevneu.2005.10.005 · Cited by 57
Partial resistance to malonate‐induced striatal cell death in transgenic mouse models of Huntington's disease is dependent on age and CAG repeat length
Hansson, O., Castilho, R. F., Korhonen, L., Lindholm, D., Bates, G. P., & Brundin, P. (2001) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2001.00482.x · Cited by 58
3‐nitropropionic acid‐induced mitochondrial permeability transition: Comparative study of mitochondria from different tissues and brain regions
Mirandola, S. R., de Melo, D. R., Saito, Â., & Castilho, R. F. (2009) · Journal of Neuroscience Research · doi:10.1002/jnr.22239 · Cited by 57
The Neuroprotective Role of Creatine
Klein, A., & Ferrante, R. J. (2007) · Springer eBooks · doi:10.1007/978-1-4020-6486-9_11 · Cited by 56
Transient Global Ischemia in Rats Yields Striatal Projection Neuron and Interneuron Loss Resembling That in Huntington's Disease
Meade, C. A., Figueredo-Cardenas, G., Fusco, F. R., Nowak, T. S., Pulsinelli, W. A., & Reiner, A. J. (2000) · Experimental Neurology · doi:10.1006/exnr.2000.7530 · Cited by 55
The neural mechanisms underlying cholinergic celldeath within the basal FOREBRAIN
Wenk, G. L., & Willard, L. B. (1998) · International Journal of Developmental Neuroscience · doi:10.1016/s0736-5748(98)00081-1 · Cited by 56
Induction of the Protective Antioxidant Response Element Pathway by 6-Hydroxydopamine In Vivo and In Vitro
Jakel, R. J., Kern, J. T., Johnson, D. A., & Johnson, J. A. (2005) · Toxicological Sciences · doi:10.1093/toxsci/kfi241 · Cited by 55
“Mitochondrial inhibition can also generate free radicals via an excitotoxic mechanism (Albin and Greenamyre, 1992; Brouillet and Beal, 1993; Srivastava et al., 1993).”
Background
Expression of metabotropic glutamate receptor 1 isoforms in the substantia nigra pars compacta of the rat
Kosinski, C., Standaert, D. G., Testa, C. M., et al. (1998) · Neuroscience · doi:10.1016/s0306-4522(97)00654-4 · Cited by 54
Selective loss of NMDA receptor NR1 subunit isoforms in Alzheimer's disease
Hynd, M., Scott, H., & Dodd, P. R. (2004) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2003.02330.x · Cited by 56
Excited to death: different ways to lose your neurones
Dodd, P. R. (2002) · Biogerontology · doi:10.1023/a:1015255312948 · Cited by 53
“Any impediment to maintaining the membrane potential might trigger an excitotoxic cascade, especially through the activation of Ca2+-dependent cellular proteases, lipases, etc (Albin and Greenamyre 1992; Dodd et al. 1994).”
Background
New findings in the ataxia of Charlevoix–Saguenay
Gazulla, J., Benavente‐Fernández, I., Vela, A. C., Marín, M. Á., Pablo, L. E., Tessa, A., Caballo, M. R. B., Santorelli, F. M., Nesti, C., Modrego, P. J., et al. (2011) · Journal of Neurology · doi:10.1007/s00415-011-6269-5 · Cited by 51
“amount of pontocerebellar fibres found in the images presented herein, it is plausible that glutamate excitotoxicity could bring about neuronal death in the cerebellar cortex [2, 21, 32].”
Background
Mitochondrial dysfunction in progressive supranuclear palsy
Albers, D. (2002) · Neurochemistry International · doi:10.1016/s0197-0186(01)00126-7 · Cited by 51
Recent advances in Huntingtonʼs disease: implications for experimental therapeutics
Feigin, A., & Zgaljardic, D. J. (2002) · Current Opinion in Neurology · doi:10.1097/00019052-200208000-00013 · Cited by 50
Regulation of microglia by glutamate and its signal pathway in neurodegenerative diseases
Zhang, X., Wang, D., Zhang, B., Zhu, J., Zhou, Z., & Cui, L. (2020) · Drug Discovery Today · doi:10.1016/j.drudis.2020.04.001 · Cited by 53
Rhes, a striatal-enriched protein, promotes mitophagy via Nix
Sharma, M., Ramírez-Jarquín, U. N., Rivera, O., Kazantzis, M., Eshraghi, M., Shahani, N., Sharma, V., Tapia, R., & Subramaniam, S. (2019) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1912868116 · Cited by 49
“It is long known that 3-NP elicits striatal-specific lesion (Beal et al., 1993; Cirillo et al., 2019), and mechanisms such as oxidative stress and excitotoxicity were implicated (Albin and Greenamyre, 1992; Beal, 2000).”
Background
Glutamate receptor abnormalities in the YAC128 transgenic mouse model of Huntington’s disease
Benn, C., Slow, E., Farrell, L. A., Graham, R. K., Deng, Y., Hayden, M. R., & Cha, J.-H. J. (2007) · Neuroscience · doi:10.1016/j.neuroscience.2007.03.010 · Cited by 50
“Glutamate receptors in HD Intrastriatal administration of exogenous glutamate receptor agonists, particularly NMDA agonists, reproduces neuropathological features of HD (Beal et al., 1986,DiFiglia, 1990,Albin and Greenamyre, 1992).”
Background
Selective vulnerability of the CA1 region of hippocampus to the indirect excitotoxic effects of malonic acid
Davolio, C., & Greenamyre, J. T. (1995) · Neuroscience Letters · doi:10.1016/0304-3940(95)11600-2 · Cited by 50
Self-citation
Excitotoxic mechanisms in the pathogenesis of dementia
Dodd, P. R., Scott, H. L., & Westphalen, R. I. (1994) · Neurochemistry International · doi:10.1016/0197-0186(94)90064-7 · Cited by 50
The Spiritual Brain: Science and Religious Experience
Newberg, A. B. (2017) · Springer series in cognitive and neural systems · doi:10.1007/978-3-319-29674-6_29 · Cited by 51
Glutamate Antagonists in Therapy of Stroke
Prass, K., & Dirnagl, U. (1998) · Restorative Neurology and Neuroscience · doi:10.3233/rnn-1998-00052 · Cited by 48
New Insights Into the Clinical Features, Pathogenesis and Molecular Genetics of Huntington Disease
Kremer, B. P. H., Weber, B. H. F., & Hayden, M. R. (1992) · Brain Pathology · doi:10.1111/j.1750-3639.1992.tb00709.x · Cited by 49
Prospects of glutamate antagonists in the therapy of Parkinson's disease
Blandini, F., & Greenamyre, J. T. (1998) · Fundamental and Clinical Pharmacology · doi:10.1111/j.1472-8206.1998.tb00918.x · Cited by 49
Self-citation
Calpain Facilitates the Neuron Death Induced by 3-Nitropropionic Acid and Contributes to the Necrotic Morphology
Pang, Z., Bondada, V., Sengoku, T., Siman, R. G., & Geddes, J. W. (2003) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/62.6.633 · Cited by 49
“Indirect excitotoxic mechanisms are strongly implicated in 3NP-toxicity (3), and 3NP-induced necrosis is exacerbated by low levels of extracellular glutamate.”
Background
Pathogenesis of brain dysfunction in Batten disease
Walkley, S. U., March, P. A., Schroeder, C. E., et al. (1995) · American Journal of Medical Genetics · doi:10.1002/ajmg.1320570218 · Cited by 49
Neuroprotective and symptomatic effects of targeting group III mG lu receptors in neurodegenerative disease
Williams, C. J., & Dexter, D. T. (2013) · Journal of Neurochemistry · doi:10.1111/jnc.12608 · Cited by 48
“In addition to dysfunctional and excessive glutamatergic signalling in certain neurodegenerative diseases, increased neuronal vulnerability of specific cell populations can result in neurotoxicity in response to normal physiological levels of glutamate (Albin and Greenamyre 1992; Beal 1992).”
Background
CSF and serum metabolic profile of patients with Huntington's chorea: A study by high resolution proton NMR spectroscopy and HPLC
Nicoli, F., Vion‐Dury, J., Maloteaux, J. M., Delwaide, C., Sylviane Confort-gouny, A., SCIAKY, M., & Cozzone, P. J. (1993) · Neuroscience Letters · doi:10.1016/0304-3940(93)90168-k · Cited by 48
Abnormal NMDA receptor function exacerbates experimental autoimmune encephalomyelitis
Grasselli, G., Rossi, S., Musella, A., Gentile, A., Loizzo, S., Muzio, L., Sanza, C. D., Errico, F., Musumeci, G., Haji, N., et al. (2012) · British Journal of Pharmacology · doi:10.1111/j.1476-5381.2012.02178.x · Cited by 47
“Glutamate toxicity has in fact been proposed as the basis of the pathogenesis of ischaemic brain damage (Arundine and Tymianski, 2004) and of several neurodegenerative diseases, including Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, amyotrophic lateral sclerosis (Albin and Greenamyre, 1992) and mult…”
Background
3‐Ureidopropionate contributes to the neuropathology of 3‐ureidopropionase deficiency and severe propionic aciduria: A hypothesis
Kölker, S., Okun, J. G., Hörster, F., Assmann, B. E., Ahlemeyer, B., Kohlmüller, D., Exner‐Camps, S., Mayatepek, E., Krieglstein, J., & Hoffmann, G. F. (2001) · Journal of Neuroscience Research · doi:10.1002/jnr.10012 · Cited by 47
“Excitotoxicity induced by primary impairment of energy metabolism has been termed ‘weak’, ‘indirect’ or ‘secondary’ (Albin and Greenamyre, 1992; Beal, 1992) in contrast to a direct overstimulation of glutamate receptors by agonists.”
Background
Reduced creatine kinase as a central and peripheral biomarker in Huntington's disease
Kim, J., Amante, D. J., Moody, J. P., Edgerly, C. K., Bordiuk, O. L., Smith, K., Matson, S. A., Matson, W. R., Scherzer, C. R., Rosas, H. D., et al. (2010) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2010.05.001 · Cited by 47
“Energetic defects in HD subjects have been chronicled for many years and include primary alterations of electron transport chain complexes [2-8].”
Striatal Damage and Oxidative Stress Induced by the Mitochondrial Toxin Malonate Are Reduced in Clorgyline-Treated Rats and MAO-A Deficient Mice
Maragos, W. F., Young, K. L., Altman, C. S., et al. (2004) · Neurochemical Research · doi:10.1023/b:nere.0000018845.82808.45 · Cited by 47
Late-onset selective neuronal damage in the rat spinal cord induced by continuous intrathecal administration of AMPA
Nakamura, R., Kamakura, K., & Kwak, S. (1994) · Brain Research · doi:10.1016/0006-8993(94)90490-1 · Cited by 47
Influence of energy deficiency on the subcellular processes of Substantia Nigra Pars Compacta cell for understanding Parkinsonian neurodegeneration
Muddapu, V. R., & Chakravarthy, V. S. (2021) · Scientific Reports · doi:10.1038/s41598-021-81185-9 · Cited by 49
Species differences in the role of excitatory amino acids in experimental parkinsonism
Fornai, F., Vaglini, F., Maggio, R., et al. (1997) · Neuroscience & Biobehavioral Reviews · doi:10.1016/s0149-7634(96)00042-5 · Cited by 46
Differential expression of kainate receptors in the basal ganglia of the developing and adult rat brain
Wüllner, U., Standaert, D. G., Testa, C. M., Penney, J. B., & Young, A. B. (1997) · Brain Research · doi:10.1016/s0006-8993(97)00645-8 · Cited by 45
Inhibitory Effects of Adenine Nucleotides on Brain Mitochondrial Permeability Transition
Saito, Â., & Castilho, R. F. (2010) · Neurochemical Research · doi:10.1007/s11064-010-0228-x · Cited by 47
Mitochondrial matters of the brain: the role in Huntington’s disease
Turner, C., & Schapira, A. H. V. (2010) · Journal of Bioenergetics and Biomembranes · doi:10.1007/s10863-010-9290-y · Cited by 45
Metabolic Abnormalities of Erythrocytes as a Risk Factor for Alzheimer's Disease
Kosenko, E. A., Tikhonova, L. A., Montoliu, C., Barreto, G. E., Aliev, G., & Kaminsky, Y. G. (2018) · Frontiers in Neuroscience · doi:10.3389/fnins.2017.00728 · Cited by 47
“The numerous studies have provided conclusive proof that glutamate becomes neurotoxic via the NMDA receptor when intracellular energy levels are reduced (Novelli et al., 1988; Beal et al., 1991; Albin and Greenamyre, 1992; Beal, 1992; Storey et al., 1992; Kosenko et al., 1994; Gonzalez et al., 2015).”
Background
Effects of MK-801 on recognition and neurodegeneration in an MPTP-induced Parkinson's rat model
Hsieh, M., Gu, S.-L., Ho, S.-C., Pawlak, C. R., Lin, C., Ho, Y., Lai, T., & Wu, F.-Y. (2012) · Behavioural Brain Research · doi:10.1016/j.bbr.2011.12.035 · Cited by 42
Electrophysiology of the neuroprotective agent riluzole on striatal spiny neurons
Centonze, D., Calabresi, P., Pisani, A., et al. (1998) · Neuropharmacology · doi:10.1016/s0028-3908(98)00081-1 · Cited by 43
Insulin affects synaptosomal GABA and glutamate transport under oxidative stress conditions
Duarte, A. I., Santos, M. S., Seiça, R. M. F., et al. (2003) · Brain Research · doi:10.1016/s0006-8993(03)02679-9 · Cited by 43
Histological and temporal characteristics of nigral transneuronal degeneration after striatal injury
DeGiorgio, L. A., Dibinis, C., Milner, T. A., Saji, M., & Volpe, B. T. (1998) · Brain Research · doi:10.1016/s0006-8993(98)00247-9 · Cited by 42
Effects of in vivo sodium azide administration on the immunohistochemical localization of kynurenine aminotransferase in the rat brain
Knyihár‐Csillik, E., Okuno, E., & Vécsei, L. (1999) · Neuroscience · doi:10.1016/s0306-4522(99)00306-1 · Cited by 42
Cellular Delivery of CNTF but not NT-4/5 Prevents Degeneration of Striatal Neurons in a Rodent Model of Huntington's Disease
Emerich, D. F. (1998) · Cell Transplantation · doi:10.1016/s0963-6897(97)00163-2 · Cited by 42
Role of protein oxidation in aging and in age-associated neurodegenerative diseases
Carney, J. M., & Carney, A. M. (1994) · Life Sciences · doi:10.1016/0024-3205(94)00390-4 · Cited by 42
Therapeutic potential of targeting glutamate receptors in Parkinson’s disease
Finlay, C. J., & Duty, S. (2014) · Journal of Neural Transmission · doi:10.1007/s00702-014-1176-4 · Cited by 41
A Computational Model of Loss of Dopaminergic Cells in Parkinson's Disease Due to Glutamate-Induced Excitotoxicity
Muddapu, V. R., Mandali, A., Chakravarthy, S. V., & Ramaswamy, S. (2019) · Frontiers in Neural Circuits · doi:10.3389/fncir.2019.00011 · Cited by 42
“The above two approaches are interrelated and not entirely independent as one form of excitotoxicity - the ‘weak excitotoxicity’ - is thought to have its roots in impaired cellular metabolism (Albin and Greenamyre, 1992).”
BackgroundInfluential
Focused ultrasound in Parkinson's disease: A twofold path toward disease modification
Foffani, G., Trigo‐Damas, I., Pineda‐Pardo, J. A., Blesa, J., Rodríguez‐Rojas, R., Martínez‐Fernández, R., & Obeso, J. A. (2019) · Movement Disorders · doi:10.1002/mds.27805 · Cited by 45
Screening Cascade and Development of Potential Positron Emission Tomography Radiotracers for mGluR5: In vitro and In vivo Characterization
Patel, S., Ndubizu, O., Hamill, T. G., Chaudhary, A., Burns, H. D., Hargreaves, R. J., & Gibson, R. E. (2005) · Molecular Imaging and Biology · doi:10.1007/s11307-005-0005-4 · Cited by 41
The early cellular pathology of Huntington’s disease
Li, X.-J. (1999) · Molecular Neurobiology · doi:10.1007/bf02742437 · Cited by 31
Serial 1H-NMR Spectroscopy Study of Metabolic Impairment in Primates Chronically Treated with the Succinate Dehydrogenase Inhibitor 3-Nitropropionic Acid
Dautry, C., Condé, F., Brouillet, E., Mittoux, V., Beal, M. F., Bloch, G., & Hantraye, P. (1999) · Neurobiology of Disease · doi:10.1006/nbdi.1999.0244 · Cited by 41
Neuroinflammation and the plasticity-related immediate-early gene Arc
Rosi, S. (2011) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2011.02.003 · Cited by 40
Age-Dependent Differences in Survival of Striatal Somatostatin–NPY–NADPH–Diaphorase-Containing Interneurons versus Striatal Projection Neurons after Intrastriatal Injection of Quinolinic Acid in Rats
Figueredo-Cardenas, G., Chen, Q., & Reiner, A. J. (1997) · Experimental Neurology · doi:10.1006/exnr.1997.6549 · Cited by 40
Expression of N-Methyl-D-Aspartate receptor subunit mRNAs in the human brain: Striatum and globus pallidus
Kosinski, C. M., Standaert, D. G., Counihan, T. J., Scherzer, C. R., Kerner, J. A., Daggett, L. P., Veli�elebi, G., Penney, J. B., Young, A. B., & Landwehrmeyer, G. B. (1998) · The Journal of Comparative Neurology · doi:10.1002/(sici)1096-9861(19980105)390:1 · Cited by 62
Ceftriaxone Prevents the Neurodegeneration and Decreased Neurogenesis Seen in a Parkinson’s Disease Rat Model: An Immunohistochemical and MRI Study
Weng, J.-C., Tikhonova, M. A., Chen, J.-H., Shen, M.-S., Meng, W.-Y., Chang, Y.-T., Chen, K.-H., Liang, K.-C., Hung, C.-S., Amstislavskaya, T. G., et al. (2016) · Behavioural Brain Research · doi:10.1016/j.bbr.2016.02.034 · Cited by 39
Target modulation of glycolytic pathways as a new strategy for the treatment of neuroinflammatory diseases
Wang, H., Liu, S., Sun, Y., Chen, C., Hu, Z., Li, Q., Long, J., Yan, Q., Liang, J., Lin, Y., et al. (2024) · Ageing Research Reviews · doi:10.1016/j.arr.2024.102472 · Cited by 39
Huntington's disease: progress and potential in the field
Stack, E. C., & Ferrante, R. J. (2007) · Expert Opinion on Investigational Drugs · doi:10.1517/13543784.16.12.1933 · Cited by 39
Neuroprotective Effects of the α2-Adrenoceptor Antagonists, (+)-Efaroxan and (±)-Idazoxan, against Quinolinic Acid-Induced Lesions of the Rat Striatum
Martel, J.-C., Chopin, P., Colpaert, F. C., & Marien, M. R. (1998) · Experimental Neurology · doi:10.1006/exnr.1998.6942 · Cited by 39

Authors: Albin, R. L., & Greenamyre, J. T.
Affiliations: University of Michigan (US)
University of Rochester (US)
ORCID: Albin, Roger L.
Greenamyre, J. Timothy
Venue: Neurology
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 1992-04
Volume: 42
Issue: 4
Pages: 733-733
ISSN: 0028-3878 (ISSN-L)
1526-632X
DOI: 10.1212/wnl.42.4.733
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

Alternative excitotoxic hypotheses

Abstract

Overview

Integrity signals

Verification

Claims the paper makes

Claims other papers make about this one

Citations

Cited by

Related

Metadata

Record

About these checks