Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Expression of chromogranin A in various neurological diseases was examined immunohistochemically using purified anti-human chromogranin A antiserum. The antibody stained dystrophic neurites in senile plaques in Alzheimer disease brain, Pick bodies and ballooned neurons in Pick's disease brain, some Lewy bodies in the substantia nigra of Parkinson's disease, and axonal swellings in various neurological conditions including Parkinson's disease, striatonigral degeneration, Shy-Drager syndrome, amyotrophic lateral sclerosis and cerebral infarction. The present study shows that expression of chromogranin A is not an exclusive feature of Alzheimer disease or Pick's disease, and indicates that it could be a useful marker for various neurological diseases.
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PMID:Expression of chromogranin A in lesions in the central nervous system from patients with neurological diseases. 804 89

We developed a new graphic method using N-isopropyl-p-[123I]iodoamphetamine (IMP) and SPECT of the brain, the graph on which all three parameters, cerebral blood flow, distribution volume (Vd) and delayed count to early count ratio (Delayed/Early ratio), were able to be evaluated simultaneously. The kinetics of 123I-IMP in the brain was analyzed by a 2-compartment model, and a standard input function was prepared by averaging the time activity curves of 123I-IMP in arterial blood on 6 patients with small cerebral infarction etc. including 2 normal controls. Being applied this method to the differential diagnosis between Parkinson's disease and progressive supranuclear palsy, we were able to differentiate both with a glance, because the distribution volume of the frontal lobe significantly decreased in Parkinson's disease (Mean +/- SD; 26 +/- 6 ml/g). This method was clinically useful. We think that the distribution volume of 123I-IMP may reflect its retention mechanism in the brain, and the values are related to amine, especially to dopamine receptors and its metabolism.
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PMID:[A new graphic method for evaluation of distribution volume on N-isopropyl-p-[123I]iodoamphetamine (IMP) SPECT]. 826 11

N-isopropyl-p[123I]iodoamphetamine (123I-IMP) SPECT and quantitative regional cerebral blood flow (rCBF) studies were performed in 111 patients with cerebral disorders. Continuous arterial blood sampling method based on the microsphere model was used as a quantitative rCBF measurement. We evaluated rCBF in patients with dementia and also in patients with poor activities of daily living (ADL). Patients with dementia showed significant reduction of mean CBF in contrast to patients without dementia. Significant decrease of rCBF in the bilateral frontal cortex, parietal cortex and basal ganglia and the right temporal cortex were found in demented patients. Although patients with vascular dementia showed decreased rCBF in bilateral basal ganglia, demented patients with Parkinson's disease showed no significant reduction of rCBF in any regions. Patients with poor ADL showed decreased rCBF in all brain regions. And particularly frontal and basal ganglionic defects were most pronounced. Patients with poor ADL resulted from cerebral infarction showed significant decrease of rCBF in bilateral basal ganglia. However, there was no significant correlation in Parkinson's disease between ADL and rCBF. The rCBF measurement with 123I-IMP is useful for clinical evaluation of demented patients and patients with poor ADL.
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PMID:[Quantitative regional cerebral blood flow study with 123I-IMP in patients with dementia and in patients with poor activities of daily living]. 827 96

We examined the immunohistochemical localization of the proinflammatory cytokines tumor necrosis factor-alpha, lymphotoxin and interferon-gamma in 22 autopsy brains of patients with either cerebrovascular disease (CVD) or other neurological diseases as well as 2 non-neurological control brains. These cytokines were coexpressed mostly in the microglia/macrophages and in a few astroglia in the brains with acute cerebral infarction and cerebral hemorrhage. In cases with cerebral infarction, they were observed as early as 33 h after the onset of the illness and persisted for up to 40 days after the onset. In one patient with cerebral hemorrhage who survived for 4 h, the cytokine-immunoreactive glial cells were confined to the margins of the hematoma. In contrast, the cytokine-immunoreactive glia were distributed diffusely in one patient with cerebral hemorrhage who died 12 days after the onset of the illness. Labeling for these cytokines was weak in the glial cells of control brains and those with neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease and multiple system atrophy, in so far as there were no concomitant acute CVD foci. The present results indicate that proinflammatory cytokines are up-regulated in the brains of patients with acute stroke, and suggest an early inflammatory response in human CVD.
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PMID:Glial expression of cytokines in the brains of cerebrovascular disease patients. 887 Aug 30

Cerebrovascular disease exemplifies the poor regenerative capacity of the CNS. While there are methods to prevent cerebral infarction, there is no effective therapy available to ameliorate the anatomical, neurochemical and behavioral deficits which follow cerebral ischemia. Focal and transient occlusion of the middle cerebral artery (MCA) in rodents has been reported to result in neuropathology similar to that seen in clinical cerebral ischemia. Using specific techniques, this MCA occlusion can result in a well-localized infarct of the striatum. This review article will provide data accumulated from animal studies using the MCA occlusion technique in rodents to examine whether neural transplantation can ameliorate behavioral and morphological deficits associated with cerebral infarction. Recent advances in neural transplantation as a treatment modality for neurodegenerative disorders such as Parkinson's disease, have revealed that fetal tissue transplantation may produce neurobehavioral recovery. Accordingly, fetal tissue transplantation may provide a potential therapy for cerebral infarction. Preliminary findings in rodents subjected to unilateral MCA occlusion, and subsequently transplanted with fetal striatal tissue into the infarcted striatum have produced encouraging results. Transplanted fetal tissue, assessed immunohistochemically, has been demonstrated to survive and integrate with the host tissue, and, more importantly, ameliorate the ischemia-related behavioral deficits, at least in the short term. Although, this review will focus primarily on cerebral ischemia, characterized by a localized CNS lesion within the striatum, it is envisioned that this baseline data may be extrapolated and applied to cerebral infarction in other brain areas.
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PMID:Neural transplantation as an experimental treatment modality for cerebral ischemia. 899 11

Omental transposition (OT) to revascularize the brain was first performed in animals in the late 1960s, where it was shown that blood vessels originating from the omentum crossed through the omental-cerebral interface prior to developing into large-sized vessels that penetrated directly and deeply into the underlying brain. The additional cerebral blood flow coming from the omentum was of sufficient volume to protect an animal's brain from cerebral infarction even in the presence of middle cerebral artery ligation. It was also learned that the omentum was a rich source for neurotransmitters and omentum-derived nerve growth substance. OT to the brain is now being done for a variety of conditions which include strokes, TIAs, epilepsy, and Parkinson's disease. Of recent interest is the published information that OT may play some role in Alzheimer's disease (AD). The placement of the omentum on an AD brain has led to a profound decrease in senile plaque formation. The omentum may ultimately prove to be beneficial in reversing or at least stabilizing the dementia associated with the devastation of AD.
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PMID:Omental transposition to the brain for Alzheimer's disease. 932 3

The authors report on a series of patients with idiopathic Parkinson's disease (IPD) who underwent stereotactic radiofrequency (RF) pallidotomies, three of whom suffered delayed postoperative strokes. These three belonged to a group consisting of 42 patients with medically intractable IPD in whom 50 pallidotomies were performed. All three patients had significant previous vascular disease and were in a high-risk group for cerebral infarction. A postoperative magnetic resonance (MR) image was obtained immediately after the pallidotomy was performed to document the placement of the RF lesion and to rule out any hematoma. The delayed strokes occurred on postoperative Days 10, 51, and 117 in patients with previous vascular disease (Group 1, 11 patients). No strokes occurred in the group with the vascular disease risk factor (Group 2, 11 patients) or in the group with no risk factors for vascular disease (Group 3, 20 patients). This observation is statistically significant (p < 0.05). The T2-weighted MR images showed the lesions as high-intensity signals extending to the posterior limb of the internal capsule ipsilateral to the pallidotomy site. The poststroke T1-weighted images obtained in two patients showed persistent contrast enhancement of the RF lesion and no enhancement around the stroke lesion. Clinically and radiographically, these discrete new lesions represent delayed infarctions, suggesting that RF lesioning can induce delayed injury in adjacent tissue. Patients with previously identified vasculopathy may be at risk for delayed capsular infarction following RF pallidotomy.
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PMID:Delayed internal capsule infarctions following radiofrequency pallidotomy. Report of three cases. 938 11

A 36 year old man, who sustained a skull fracture in 1984, was unconscious for 24 hours, and developed signs of Parkinson's syndrome 6 weeks after the injury. When assessed in 1995, neuroimaging disclosed a cerebral infarction due to trauma involving the left caudate and lenticular nucleus. Parkinson's syndrome was predominantly right sided, slowly progressive, and unresponsive to levodopa therapy. Reaction time tests showed slowness of movement initiation and execution with both hands, particularly the right. Recording of movement related cortical potentials suggested bilateral deficits in movement preparation. Neuropsychological assessment disclosed no evidence of major deficits on tests assessing executive function or working memory, with the exception of selective impairments on the Stroop and on a test of self ordered random number sequences. There was evidence of abulia. The results are discussed in relation to previous literature on basal ganglia lesions and the effects of damage to different points of the frontostriatal circuits.
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PMID:Parkinson's syndrome after closed head injury: a single case report. 1008 39

We describe six patients with classical levodopa-responsive Parkinson's disease (PD) and one case of levodopa-responsive familial juvenile dystonia-parkinsonism with fixed contractures of the hands, feet or legs. In most patients contractures became established over a short period (2 months-2 years) but a considerable time after onset of parkinsonism (mean 13 years). Mean disease duration was 17 years, and all patients had severe levodopa-induced dyskinesias, either biphasic or peak dose, in the affected limb prior to onset of the contracture. Nerve conduction studies excluded peripheral ulnar nerve lesions in all patients with one exception, who was found to have a mild bilateral ulnar entrapment neuropathy. Transcranial magnetic stimulation performed in five of the seven patients showed shorter mean central motor conduction time in the affected than in the unaffected limb. Results of magnetic resonance imaging of the brain performed in a subgroup of patients were normal, with no evidence to suggest multiple system atrophy, cerebral infarction or focal abnormalities of the basal ganglia. We conclude that hand and feet contractures are not necessarily restricted to parkinson plus syndromes and may complicate otherwise typical PD in the absence of a structural or peripheral nervous cause. Striatal dopaminergic deficiency, particularly long-standing, may have a role in the pathogenesis of limb contractures in PD.
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PMID:Limb contractures in levodopa-responsive parkinsonism: a clinical and investigational study of seven new cases. 1046 Apr 43

We evaluated the effect of nicergoline on superoxide production by rat microglias using a 2-methyl-6-(p-methoxyphenyl)-3, 7-dihydroimidazo[1,2-a]pyrazin-3-one-dependent chemiluminescence assay. Nicergoline dose-dependently inhibited superoxide production by microglias stimulated with phorbol myristate acetate or opsonized zymosan, while it had no effect on superoxide production by a hypoxanthine-xanthine oxidase system. These results indicate that nicergoline does not have a scavenging effect, but has an inhibitory effect on superoxide generation by microglias. Although this drug is commonly used for treating chronic cerebral infarction, it may also have a protective effect on progression of Parkinson's disease or Alzheimer's disease.
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PMID:Inhibitory effect of nicergoline on superoxide generation by activated rat microglias measured using a simple chemiluminescence method. 1111 71


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