Disease relevance of Striatonigral Degeneration

• Met-enkephalin immunoreactivity in the basal ganglia in Parkinson's disease and striatonigral degeneration [1].
• A case of probable neuroleptic malignant syndrome (NMS) complicating L-dopa withdrawal in striatonigral degeneration is described [2].
• In the present experiment we studied the ability of embryonic striatal grafts to protect against striatal quinolinic acid (QA)-induced excitotoxicity in a previously established double lesion rat model of striatonigral degeneration (SND), the neuropathological substrate of parkinsonism associated with multiple system atrophy (MSA) [3].
• Similar findings were found in MSA-C and MSA-P cases (olivopontocerebellar atrophy and striatonigral degeneration types, respectively), thus indicating possible abnormal interactions of alpha-synuclein and rab3a in diseased brains [4].
• The activity of tryptophan hydroxylase was measured in nine regions of human brains from controls and patients with Parkinson's disease, striatonigral degeneration, Shy-Drager syndrome and progressive supranuclear palsy by high performance liquid chromatography with fluorescence detection [5].

Psychiatry related information on Striatonigral Degeneration

• We measured the activity of glutathione peroxidase in autopsied brain regions of neurologically normal adults and in brain of patients with primary degenerative disorder Alzheimer's type (AD/SDAT), as well as two other neurodegenerative disorders, namely Huntington's disease and striatonigral degeneration [6].

High impact information on Striatonigral Degeneration

• Normalized glucose metabolism was significantly reduced in the caudate (p < 0.03) and putamen (p < 0.003) as compared with that in normal and PD control subjects, and discriminated patients with striatonigral degeneration from control subjects (p < 0.002) [7].
• These results suggest that quantitative 18F-fluorodeoxyglucose positron emission tomography techniques may be useful in supporting a diagnosis of striatonigral degeneration in life, and in objectively assessing disease severity and potential therapeutic interventions [7].
• Nine positron emission tomography studies of regional cerebral glucose metabolism were performed in 7 patients with probable striatonigral degeneration, a disorder characterized by parkinsonian features and absent or poor response to L-dopa [8].
• These results suggest that positron emission tomography with [18F]fluorodeoxyglucose may provide an index of cell and processes degeneration in the striatum in striatonigral degeneration and is able to detect functional deficits in frontal cortex [8].
• MPTP potentiates 3-nitropropionic acid-induced striatal damage in mice: reference to striatonigral degeneration [9].

Chemical compound and disease context of Striatonigral Degeneration

• When compared with values obtained in normal volunteers, mean cerebral glucose metabolism was slightly reduced in subjects with striatonigral degeneration who, in addition, had a marked (20.5%, +/- 3 SD) relative hypometabolism in putaminal and caudate nuclei [8].
• Striatal dopamine D1 receptors were investigated in 11 patients with Parkinson's disease (PD), five patients with striatonigral degeneration (SND) and six age-matched controls by positron emission tomography and carbon-11 labelled SCH23390 [10].
• Simultaneous intrastriatal 6-hydroxydopamine and quinolinic acid injection: a model of early-stage striatonigral degeneration [11].
• A 'single toxin-double lesion' rat model of striatonigral degeneration by intrastriatal 1-methyl-4-phenylpyridinium ion injection: a motor behavioural analysis [12].
• We developed a primate model of striatonigral degeneration (SND), the neuropathology underlying levodopa-unresponsive parkinsonism associated with multiple systemic atrophy (MSA-P), by sequential systemic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 3-nitropropionic acid (3NP) in a Macaca fascicularis monkey [13].

Anatomical context of Striatonigral Degeneration

• Decreased glucose utilization in the striatum and frontal lobe in probable striatonigral degeneration [8].

Gene context of Striatonigral Degeneration

• TH activity has also been shown to be decreased in striatonigral degeneration and Shy-Drager syndrome [14].
• SPECT scans using [123I]beta-CIT (for DAT) and [123I]IBF (for D2) were performed in 18 patients with PD (12 dopa-naïve and 6 on levodopa and/or dopamine agonists), 7 with MSA of the striatonigral degeneration type, 6 with PSP, and 29 normal controls [15].
• Dystonia is predictive of subsequent altered dopaminergic responsiveness in a chronic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine+3-nitropropionic acid model of striatonigral degeneration in monkeys [16].
• We investigated whether the CGH-test can identify individual patients in the early stages of PD (n = 21) and Striatonigral Degeneration (SND, n = 11), a particular variety of MSA [17].
• Failure of caspase inhibition in the double-lesion rat model of striatonigral degeneration (multiple system atrophy) [18].

Analytical, diagnostic and therapeutic context of Striatonigral Degeneration

• We used 3-nitropropionic acid to create a rat model of advanced striatonigral degeneration in order to assess the effects of embryonic allografts upon rotational and complex-motor behavioural abnormalities [19].

References