Search Results - "Beal, M.F."

O.022 Therapeutic approaches to mitochondrial dysfunction in Parkinson's disease by Beal, M.F

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Influence of mitochondrial enzyme deficiency on adult neurogenesis in mouse models of neurodegenerative diseases by Calingasan, N.Y, Ho, D.J, Wille, E.J, Campagna, M.V, Ruan, J, Dumont, M, Yang, L, Shi, Q, Gibson, G.E, Beal, M.F

“…Abstract Mitochondrial defects including reduction of a key mitochondrial tricarboxylic acid cycle enzyme α-ketoglutarate–dehydrogenase complex (KGDHC) are…”
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Impaired brain creatine kinase activity in Huntington's disease by Zhang, S F, Hennessey, T, Yang, L, Starkova, N N, Beal, M F, Starkov, A A

“…Huntington's disease (HD) is associated with impaired energy metabolism in the brain. Creatine kinase (CK) catalyzes ATP-dependent phosphorylation of creatine…”
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Tissue inhibitors of matrix metalloproteinases are elevated in cerebrospinal fluid of neurodegenerative diseases by Lorenzl, S, Albers, D.S, LeWitt, P.A, Chirichigno, J.W, Hilgenberg, S.L, Cudkowicz, M.E, Beal, M.F

“…Matrix metalloproteinases (MMPs) are implicated in the pathogenesis of diseases such as Alzheimer's Disease (AD) and amyotrophic lateral sclerosis (ALS)…”
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Mitochondrial DNA mutations in complex I and tRNA genes in Parkinson's disease by SIMON, D. K, MAYEUX, R, MARDER, K, KOWALL, N. W, BEAL, F, JOHNS, D. R

“…To identify mitochondrial DNA (mtDNA) mutations that predispose to PD. Mitochondrial complex I activity is deficient in PD. mtDNA mutations may account for the…”
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Neuroprotective strategies for treatment of lesions produced by mitochondrial toxins: Implications for neurodegenerative diseases by Schulz, J.B., Matthews, R.T., Henshaw, D.R., Beal, M.F.

“…Neuronal death in neurodegenerative diseases may involve energy impairment leading to secondary excitotoxicity, and free radical generation. Potential…”
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Excitotoxins, Aging, and Environmental Neurotoxins: Implications for Understanding Human Neurodegenerative Diseases by Dawson, R., Beal, M.F., Bondy, S.C., Dimonte, D.A., Isom, G.E.

“…We are an aging society and current demographic trends point to a likely increase in age-related neurodegenerative diseases. The aged population may have a…”
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Mitochondrial pathology and muscle and dopaminergic neuron degeneration caused by inactivation of Drosophila Pink1 is rescued by Parkin by Yang, Y, Gehrke, S, Imai, Y, Huang, Z, Ouyang, Y, Wang, J.W, Yang, L, Beal, M.F, Vogel, H, Lu, B

“…Mutations in Pink1, a gene encoding a Ser/Thr kinase with a mitochondrial-targeting signal, are associated with Parkinson's disease (PD), the most common…”
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Inactivation of Drosophila DJ-1 leads to impairments of oxidative stress response and phosphatidylinositol 3-kinase/Akt signaling by Yang, Y, Gehrke, S, Haque, M.E, Imai, Y, Kosek, J, Yang, L, Beal, M.F, Nishimura, I, Wakamatsu, K, Ito, S

“…Parkinson's disease (PD) is the most common movement disorder characterized by dopaminergic dysfunction and degeneration. The cause of most PD cases is…”
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Aluminum-induced neurofibrillary degeneration affects a subset of neurons in rabbit cerebral cortex, basal forebrain and upper brainstem by Kowall, N W, Pendlebury, W W, Kessler, J B, Perl, D P, Beal, M F

“…Neurofibrillary tangles in Alzheimer's disease show a predilection for cortical pyramidal and subcortical projection neurons. The antigenic composition,…”
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Oxidative stress in patients with Friedreich ataxia by SCHULZ, J. B, DEHMER, T, BOGDANOV, M. B, SCHÖLS, L, MENDE, H, HARDT, C, VORGERD, M, BÜRK, K, MATSON, W, DICHGANS, J, BEAL, M. F

“…Increased generation of reactive oxygen species may underlie the pathophysiology of Friedreich ataxia (FRDA). The authors measured concentrations of…”
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Increased CSF F 2 -isoprostane concentration in probable AD by Montine, T.J., Beal, M.F., Cudkowicz, M.E., O’Donnell, H., Margolin, R.A., McFarland, L., Bachrach, A.F., Zackert, W.E., Roberts, L.J., Morrow, J.D.

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Familial multisystem degeneration with parkinsonism associated with the 11778 mitochondrial DNA mutation by SIMON, D. K, PULST, S. M, SUTTON, J. P, BROWNE, S. E, BEAL, M. F, JOHNS, D. R

“…To investigate a family with maternally inherited, adult-onset multisystem degeneration including prominent parkinsonism to determine whether clinical features…”
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Oral dyskinesias and histopathological alterations in substantia nigra after long-term haloperidol treatment of old rats by Andreassen, O.A, Ferrante, R.J, Aamo, T.O, Beal, M.F, Jørgensen, H.A

“…The pathophysiologic basis of tardive dyskinesia remains unclear, but several lines of evidence suggest that persistent neuronal changes in the basal ganglia…”
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Cerebrospinal fluid F 2 -isoprostanes are elevated in Huntington’s disease by Montine, T.J., Beal, M.F., Robertson, D., Cudkowicz, M.E., Biaggioni, I., O’Donnell, H., Zackert, W.E., Roberts, L.J., Morrow, J.D.

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In vivo neurotoxicity of beta-amyloid [beta(1-40)] and the beta(25-35) fragment by Kowall, N W, McKee, A C, Yankner, B A, Beal, M F

“…We examined the histological changes produced by injections of beta-amyloid [beta(1-40)], and control peptides in rat and monkey cerebral cortex. beta(25-35)…”
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Mitochondrial DNA variants observed in Alzheimer disease and Parkinson disease patients by Shoffner, J M, Brown, M D, Torroni, A, Lott, M T, Cabell, M F, Mirra, S S, Beal, M F, Yang, C C, Gearing, M, Salvo, R

“…Mitochondrial DNA (mtDNA) variants associated with Alzheimer disease (AD) and Parkinson disease (PD) were sought by restriction endonuclease analysis in a…”
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Free radicals and aging by Beal, M.F.

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Manganese injection into the rat striatum produces excitotoxic lesions by impairing energy metabolism by Brouillet, E P, Shinobu, L, McGarvey, U, Hochberg, F, Beal, M F

“…There is compelling evidence that excessive exposure to manganese (Mn) produces neurotoxicity, especially in the basal ganglia, resulting in a dystonic…”
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Reduction of post-traumatic brain injury and free radical production by inhibition of the caspase-1 cascade by Fink, K.B., Andrews, L.J., Butler, W.E., Ona, V.O., Li, M., Bogdanov, M., Endres, M., Khan, S.Q., Namura, S., Stieg, P.E., Beal, M.F., Moskowitz, M.A., Yuan, J., Friedlander, R.M.

“…Necrotic and apoptotic cell death both play a role mediating tissue injury following brain trauma. Caspase-1 (interleukin-1β converting enzyme) is activated…”
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