Does impairment of energy metabolism result in excitotoxic neuronal death in neurodegenerative illnesses?

Annals of Neurology

Volumn 31, Issue 2, 1992, Pages 119-130

  Beal, M Flint ^a  

^a MASSACHUSETTS GENERAL HOSPITAL   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

AMINO ACID RECEPTOR BLOCKING AGENT; EXCITATORY AMINO ACID; EXCITOTOXIN; GLUTAMIC ACID; N METHYL DEXTRO ASPARTIC ACID RECEPTOR; N METHYL DEXTRO ASPARTIC ACID RECEPTOR BLOCKING AGENT; PYRIDINE DERIVATIVE;

AGING; ALZHEIMER DISEASE; AMYOTROPHIC LATERAL SCLEROSIS; BIOENERGY; ENCEPHALOMYOPATHY; ENERGY METABOLISM; HUNTINGTON CHOREA; MITOCHONDRIAL ENERGY TRANSFER; MITOCHONDRIAL RESPIRATION; NERVE CELL NECROSIS; NERVE DEGENERATION; OXIDATIVE PHOSPHORYLATION; PARKINSON DISEASE; PRIORITY JOURNAL; REVIEW;

AGING; ALZHEIMER DISEASE; ANIMAL; BRAIN DISEASES; CELL DEATH; ENERGY METABOLISM; GLUTAMATES; GLUTAMIC ACID; HUMAN; HUNTINGTON DISEASE; ION CHANNEL GATING; MITOCHONDRIA; MODELS, BIOLOGICAL; MPTP POISONING; NERVE DEGENERATION; NEURONS; NEUROTOXINS; OXIDATIVE PHOSPHORYLATION; PARKINSON DISEASE; PARKINSON DISEASE, SECONDARY; PRIMATES; RATS; RECEPTORS, N-METHYL-D-ASPARTATE; SUPPORT, U.S. GOV'T, P.H.S.;

EID: 0026584524     PISSN: 03645134     EISSN: 15318249     Source Type: Journal    
DOI: 10.1002/ana.410310202     Document Type: Article

References (174)

1. Glutamate neurotoxicity and diseases of the nervous system
2. Mitochondrial electron transport and oxidative phosphorylation system
3. Mitochondrial genes and disease
4. Mitochondrial protein import
5. An autosomal dominant disorder with multiple deletions of mitochondrial DNA starting at the D‐loop region
6. Evidence in a lethal infantile mitochondrial disease for a nuclear mutation affecting respiratory complexes I and IV
7. The role of mitochondrial DNA in Huntington's disease
8. Patterns of inheritance of the symptoms of Huntington's disease suggestive of an effect of genomic imprinting
9. 18FDG and computed tomographic scan
10. Positron emission tomography in the early diagnosis of Huntington's disease
11. Reduced cerebral glucose metabolism in asymptomatic subjects at risk for Huntington's disease
12. Normal caudate glucose metabolism in persons at risk for Huntington's disease
13. The combined use of positron emission tomography and DNA polymorphisms for preclinical detection of Huntington's disease
14. A comparison of neurological, metabolic, structural and genetic evaluations in persons at risk for Huntington's disease
15. Cortical and subcortical glucose consumption measured by PET in patients with Huntington's disease
16. Decreased pyruvate dehydrogenase complex activity in Huntington and Alzheimer brain
17. Distribution of phosphate‐activated glutaminase, succinic dehydrogenase, pyruvate dehydrogenase, and α‐glutamyl transpeptidase in post‐mortem brain from Huntington's disease and agonal cases
18. Mitochondrial function and parental sex effect in Huntington's disease
19. Evidence for a defect in NADH: ubiquinone oxidoreductase (complex I) in Huntington's disease
20. Regional mitochondrial respiratory activity in Huntington's disease brain
21. Molecular defects of NADH‐ubiquinone oxidoreductase (complex I) in mitochondrial diseases
22. Extraneuronal metabolism in early Huntington's disease
23. Luft's disease; further biochemical and ultrastructural studies of skeletal muscle in the second case
24. A case of severe hypermetabolism of nonthyroid origin with a defect in the maintenance of mitochondrial respiratory control—a correlated clinical, biochemical, and morphological study
25. Positron emission tomography in Alzheimer's disease
26. Neocortical metabolic abnormalities precede non‐memory cognitive deficits in early Alzheimer‐type dementia
27. Enzyme activities in relation to pH and lactate in postmortem brain in Alzheimer‐type and other dementias
28. Energy metabolism in disorders of the nervous system
29. Cytochrome oxidase deficiency in Alzheimer's disease
30. Mechanism of the neurotoxicity of MPTP
31. MPTP‐induced neurotoxicity and the quest for a preventative therapy for Parkinson's disease
32. +) and its analogs with the rotenone/piericidin binding site of NADH dehydrogenase
33. 1 reductase (complex I) deficiency in Parkinson's disease
34. Mitochondrial complex I deficiency in Parkinson's disease
35. Electron transport chain abnormalities in idiopathic Parkinson's disease
36. Parkinson's disease: a systemic disorder of mitochondrial oxidative phosphorylation
37. Deficiencies in complex I subunits of the respiratory chain in Parkinson's disease
38. Increase of deleted mitochondrial DNA in the striatum in Parkinson's disease and senescence
39. Quantitative determination of deleted mitochondrial DNA relative to normal DNA in parkinsonian striatum by a kinetic PCR analysis
40. Mitochondrial DNA in postmortem brain from patients with Parkinson's disease
41. Mitochondrial gene mutation: the aging process and degenerative diseases
42. Cerebellar and brainstem hypometabolism in olivopontocerebellar atrophy detected with positron emission tomography
43. Cerebral glucose hypermetabolism in Friedrich's ataxia detected with positron emission tomography
44. Abnormal glutamate metabolism in an adult‐onset degenerative neurological disorder
45. Cortical motorsensory hypometabolism in amyotrophic lateral sclerosis: a PET study
46. Lowered cerebral glucose utilization in amyotrophic lateral sclerosis
47. Experimental demyelination of the central nervous system. 3. Poisoning with potassium cyanide, sodium azide, hydroxylamine, narcotics, carbon monoxide, etc., with some consideration of bilateral necrosis occurring in the basal nuclei
48. Experimental striatal necrosis induced by sodium azide
49. Brain metabolism in vivo II
50. Choreoathetosis and striopallidal necrosis due to sodium azide
51. 3‐Nitropropionic acid‐abundant xenobiotic excitotoxin linked to putaminal necrosis and tardive dystonia
52. Basal ganglia degeneration, myelin alterations, and enzyme inhibition induced in mice by the plant toxin 3‐nitropropanoic acid
53. Nature and distribution of brain lesions in rats intoxicated with 3‐nitropropionic acid: a type of hypoxic (energy deficient) brain damage
54. Cyanide‐induced parkinsonism: clinical, MRI, and 6‐fluorodopa PET studies
55. Cyanide induced parkinsonism: a clinicopathologic report
56. Neurological disease and mitochondrial genes
57. Movement disorders in mitochondrial myopathies
58. Mitochondrial DNA mutation associated with Leber's hereditary optic neuropathy
59. A defect in mitochondrial electron‐transport activity (NADH‐coenzyme Q oxidoreductase) in Leber's hereditary optic neuropathy
60. Leber's disease and dystonia: a mitochondrial disease
61. A mutation in the tRNA Leu (UUR) gene associated with the MELAS subgroup of mitochondrial encephalomyopathies
62. A point mutation in the mitochondrial tRNA Leu (UUR) gene in MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke‐like episodes)
63. Myoclonic epilepsy and ragged‐red fiber disease (MERRF) is associated with a mitochondrial DNA tRNA Lys mutation
64. Myoclonus epilepsy associated with ragged‐red fibers (mitochondrial abnormalities): disease entity or a syndrome
65. Myoclonus epilepsy and ragged‐red fibers (MERRF). 1. A clinical, pathological, biochemical, magnetic resonance spectrographic and positron tomographic study
66. Myoclonic epilepsy and ragged‐red fibers with cytochrome oxidase deficiency: neuropathology, biochemistry, and molecular genetics
67. Neuropathology of myoclonus epilepsy associated with ragged‐red fibers (Fukuhara's disease)
68. Mitochondrial encephalomyopathies: a correlation between neuropathological findings and defects in mitochondrial DNA
69. In vivo magnetic resonance spectroscopy of brain and muscle in a type of mitochondrial encephalomyopathy (MERRF)
70. Isolation and properties of cytochrome c oxidase from rat liver and quantification of immunological differences between isoenzymes from various rat tissues with subunit‐specific antisera
71. Tissue specificity and defects in human cytochrome c oxidase
72. Isoforms of mammalian cytochrome c oxidase: correlation with human cytochrome c oxidase deficiency
73. CDNA sequence of a human skeletal muscle ADP/ATP translocator: lack of a leader peptide, divergence from a fibroblast translocator cDNA, and coevolution with mitochondrial DNA genes
74. Two distinct genes for ADP/ATP adult human liver
75. Mtdna depletion with variable tissue expression: a novel genetic abnormality in mitochondrial diseases
76. Leber hereditary optic neuropathy: involvement of the mitochondrial ND 1 gene and evidence for a intragenic suppressor mutation
77. Brain lesion, obesity and other disturbances in mice treated with monosodium glutamate
78. Lesions of striatal neurons with kainic acid provides a model for Huntington's chorea
79. Duplication of biochemical changes of Huntington's chorea by intrastriatal injections of glutamic and kainic acids
80. Kowall NW, Beal MF, et al. Selective sparing of a class of striatal neurons in Huntington's disease
81. Emson PL. Survival of basal ganglia neuropeptide Y–somatostatin neurons in Huntington's disease
82. Sparing of acetyl‐cholinesterase‐containing striatal neurons in Huntington's disease
83. Excitotoxin lesions do not mimic the alteration of somatostatin in Huntington's disease
84. Quinolinic acid: an endogenous metabolite that produces axon‐sparing lesions in rat brain
85. Replication of the neurochemical characteristics of Huntington's disease by quinolinic acid
86. Differential sparing of somatostatin–neuropeptide Y and cholinergic neurons following striatal excitotoxic lesions
87. No evidence for preservation of somatostatin containing neurons after intrastriatal injections of quinolinic acid
88. Quinolinic acid does not spare striatal neuropeptide Y–immunoreactive neurons
89. Cultured striatal neurons containing NADPH‐diaphorase or acetylcholinesterase are selectively resistant to injury by NMDA receptor agonists
90. Neurons containing NADPH‐diaphorase are selectively resistant to quinolinate toxicity
91. Relative resistance to quinolinic acid toxicity of neurons containing nicotinamide adenine dinucleotide phosphate diaphorase (NADPH‐d) in cultures of rat corticostriatal system
92. Homocysteic acid striatal lesions spare somatostatin–neuropeptide Y–NADPH‐diaphorase neurons
93. Quinolinic acid striatal lesions in primates as a model of Huntington's disease
94. Chronic quinolinic acid lesions in rats closely mimic Huntington's disease
95. Differential sensitivity of calbindin and parvalbumin immunore‐active cells in the striatum to excitotoxins
96. Parvalbumin immunoreactive neurons resist degeneration in Huntington's disease striatum
97. Regulation of neurotensin‐containing neurons in the rat striatum, effects of unilateral striatal lesions with quinolinic acid and ibotenic acid on neurotensin content and its binding site density
98. Synaptic localization of striatal NMDA, quisqualate and kainate receptors
99. Alterations of muscarinic cholinergic receptors in the rat striatum after kainic acid injections
100. 2 sites in rat caudate‐putamen: localization to intrinsic neurons and not to neocortical afferents
101. Loss of striatal serotonin synaptic receptor binding induced by kainic acid lesions: correlations with Huntington's disease
102. Effects of chronic striatal kainate lesions on some dopaminergic parameters and enkephalin immunoreactive neurons in the basal ganglia
103. GABA and benzodiazepine receptors in basal ganglia function
104. Long‐term sequelae of striatal kainate lesions
105. Functional neuronal replacment of grafted striatal neurons in the ibotenic acid–lesioned rat striatum
106. Graft‐induced behavioral recovery in an animal model of Huntington's disease
107. The QA model of Huntington's disease: locomotor abnormalities
108. Impaired learning and memory after kainic acid lesions of the striatum, a behavior model of Huntington's disease
109. Reversal of long‐term locomotor abnormalities in the kainic acid model of Huntington's disease by day 18 fetal striatal implants
110. A primate model of Huntington's disease: behavioral and anatomical studies of unilateral excitotoxic lesions of the caudate‐putamen and in the baboon
111. Choreic movements induced by unilateral kainate lesion of the striatum and L‐dopa administration in monkey
112. NMDA receptor losses in putamen from patients with Huntington's disease
113. Excitatory amino acid receptor populations in Huntington's disease
114. Abnormalities of striatal projection neurons and N‐methyl‐D‐aspartate receptors in presymptomatic Huntington's disease
115. Guam amyotrophic lateral sclerosis–parkinsonism dementia linked to a plant excitant neurotoxin
116. Brain glutamate deficiency in ALS
117. Abnormal excitatory amino acid metabolism in amyotrophic lateral sclerosis
118. The neuroexcitotoxic amino acids glutamate and aspartate are altered in the spinal cord and brain in amyotrophic lateral sclerosis
119. Amyotrophic lateral sclerosis: amino acid levels in plasma and cerebrospinal fluid
120. Neurotrophic and neurotoxic effects of amyloid β protein: reversal by tachykinin neuropeptides
121. Neurodegenerative effects of β amyloid in the adult brain and protection by substance P
122. β‐Amyloid protein increases the vulnerability of cultured cortical neurons to excitotoxic damage
123. Glutamate, glutaminase and taurine immunoreactive neurons develop neurofibrillary tangles in Alzheimer's disease
124. Quantitative morphology and regional laminar distributions of senile plaques in Alzheimer's disease
125. Anatomical correlates of the pathological changes in the neocortex in Alzheimer's disease
126. Alterations in L‐glutamate binding in Alzheimer's and Huntington's disease
127. 3H] glutamate binding
128. Normal oxidative damage to mitochondrial and nuclear DNA is extensive
129. Mitochondrial DNA mutations as an important contribution to aging and degenerative diseases
130. Decline in skeletal muscle mitochondrial respiratory chain function: possible factor in aging
131. Calcium fluxes, calcium antagonists, and calcium‐related pathology in brain ischemia, hypoglycemia and spreading depression: a unifying hypothesis
132. Calcium transport and buffering in neurons
133. Calcium‐mediated neurotoxicity: relationship to specific channel types and role in ischemic damage
134. Glutamate becomes neurotoxic via the N‐methyl‐D‐aspartate receptor when intracellular energy levels are reduced
135. The role of specific ions in glutamate neurotoxicity
136. Potassium channel activators abolish excitotoxicity in cultured hippocampal pyramidal neurons
137. Chemically induced hypoglycemia and anoxia: relationship to glutamate receptor‐mediated toxicity in retina
138. Mechanisms underlying initiation of excitotoxicity associated with metabolic inhibition
139. Tonic activation of NMDA receptors by ambient glutamate enhances excitability of neurons
140. Differential activation of glutamate receptors by spontaneously released transmitter in slices of cortex
141. Rat brain slices produce and liberate kynurenic acid upon exposure to L‐kynurenine
142. Cerebral synthesis and release of kynurenic acid, an endogenous antagonist of excitatory amino acid receptors
143. Aminooxyacetic acid results in excitotoxin lesions by a novel indirect mechanism
144. Chemical shift imaging of focal neurochemical lesions in rat brains
145. Evidence that aspartate aminotransferase activity and ketodicarboxylate carrier function are essential for the biosynthesis of transmitter glutamate
146. Influence of the malate‐aspartate shuttle on oxidative metabolism in synaptosomes
147. Phosphorylation coupled to oxidation of dihydrodiphosphopyridine nucleotide
148. Use of β‐methylene‐D, L‐aspartate to assess the role of aspartate aminotransferase in cerebral oxidative metabolism
149. Aminooxyacetic acid inhibits the malate‐aspartate shuttle in isolated nerve terminals and prevents the mitochondria from utilizing glycolytic substrates
150. Amino‐oxyacetic acid produces excitotoxic lesions in the rat striatum
151. The MPTP model: versatile contributions to the treatment of idiopathic Parkinson's disease
152. + within the monoamine systems of the primate brain following MPTP administration: an in vivo autoradiographic study
153. Rapid ATP loss caused by 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine in mouse brain
154. + neurotoxicity by N‐methyl‐D‐aspartate antagonists
155. + produces excitotoxic lesions in rats
156. Sequence of metabolic, clinical, and histological events in experimental thiamine deficiency
157. Brain mitochondrial metabolism in experimental thiamine deficiency
158. Protective effects of the glutamate antagonist MK‐801 on pyrimethamine‐induced lesions and amino acid changes in rat brain
159. Cerebral protection by barbiturate anesthesia after middle cerebral artery occlusion in Java monkeys
160. Barbiturate‐induced coma therapy for focal cerebral ischemia: effect after temporary and permanent MCA occlusions
161. + neurotoxicity: oxyradical and mitochondrial inhibitor hypotheses
162. Selective sparing of NADPH‐diaphorase neurons in neonatal hypoxia‐ischemia
163. Selective sparing of NADPH‐diaphorase–somatostatin–neuropeptide Y neurons in ischemic gerbil striatum
164. Ischemic damage in the striatum of adult gerbils: relative sparing of somatostatinergic and cholinergic neurons contrasts with loss of efferent neurons
165. Therapy of mitochondrial disorders
166. 10 therapy for a mitochondrial encephalomyopathy with cytochrome c oxidase deficiency
167. 10 and idebenone
168. Deficiency of subunits of complex I and mitochondrial encephalomyopathy
169. Ubidecarenone in the treatment of mitochondrial myopathies: a multi‐center double‐blind trial
170. 1 oxidorectase (complex I) deficiency: variable expression and possible treatment
171. Successful treatment of pure myopathy, associated with complex I deficiency with riboflavin and carnitine
172. Methods for antagonizing glutamate neurotoxicity
173. Effect of NMDA and strychnine‐insensitive glycine site antagonists on NMDA‐mediated convulsions and learning
174. Selective blockade of N‐methyl‐D‐aspartate (NMDA)‐induced convulsions by NMDA antagonists and putative glycine antagonists: relationship with phencyclidine‐like behavioral effects