ABSTRACT
Parkinson’s disease (PD) is a chronic neurological disorder of the nervoussystem, initiated by lessened production of dopamine (DA) in the substantia nigra, itaffects circa 50 percent more men than women. Theories reveal that age, genetic andenvironmental factors are involved in PD etiology but age seems to be the mostprominent risk factor. Monoamine oxidase B (MAO-B) play prominent role in theoxidative deamination of DA in the striatum. Inhibition of MAO-B in the brain maydecrease the exhaustion of DA stores and increase endogenous DA level. Glide-XPdocking, Quantum-mechanics Polarized Ligand Docking (QPLD), pharmacokineticstudies and biological activity prediction studies were utilized to explain the bindingmode, molecular interaction, inhibitory potential and pharmacokinetic properties ofTraditional Chinese Medicine (TCM) compounds on MAO-B and compared to standarddrugs used for treatment of PD, selegiline and rasagiline. Molecular docking resultsshowed Rutaecarpine and Chrysophanol to have relatively better inhibitory activitiesthan selegiline and rasagiline. Pharmacokinetic studies revealed that Rutaecarpine andChrysophanol show comparative result with selegiline and rasagiline. Also,Rutaecarpine and Chrysophanol PASS prediction for their monoamine inhibitoryactivity showed greater Pa than Pi value. Our results have shown that Rutaecarpine andChrysophanol can be a better therapeutic candidate in the treatment of PD.
ABSTRACT
Fahr's syndrome (or Fahr's disease) involves progressive calcific deposition in the wall of blood vessels of the basal ganglia and dentate nuclei of the cerebellum in young and middle-age persons. It is occasionally associated with mental retardation and extrapyramidal symptoms. Clinically it may present with an array of movement disorders, dementia and other behavioural disturbances1. We report a case of 29-year-old female with increasing frequency of seizures. Brain CT showed symmetrical calcification in basal ganglia The clinical and radiological features in our case point towards this uncommon disorder.
ABSTRACT
Objective ToinvestigatethepatternsofbrainactivityabnormalitiesinpatientswithParkinson’sdisease(PD)with freezingofgait(FOG),andtoexploretheneuropathologicalmechanismofFOG.Methods Resting-statefunctionalMRI(rs-fMRI) scanswereobtainedfrom31PDpatientsand16healthycontrols(HCs).Accordingtothefreezingofgaitquestionnaire(FOG-Q),31 PDpatientsweredividedinto15PDFOG(+)and16PDFOG(－).ANCOVAandPost-Hocttestwereperformedtoassessinter groupdifferenceofbrainactivityabnormalitybasedonregionalhomogeneity.Results ComparedtoHCs,PDFOG(+)showeddecreased ReHointheleftinferiortemporalgyrus,rightlingual,bilateralfusiform,rightoccipitalgyrus,rightcalcarine,andrightcerebellum, whileincreasedReHointherightmiddlefrontalgyrus,rightsuperiorfrontalgyrus,rightprecentralgyrus,andrightsupplementary motorarea(SMA).ComparedtoPDFOG(－),PDFOG(+)exhibitedincreasedReHointherightprecentralgyrus,rightmiddle frontalgyrus,rightinferiorfrontalgyrus,andrightSMA,whiledecreasedReHoinleftfusiform.Conclusion Thisstudysuggests thatFOGinPDisassociatedwithabnormalitiesincerebellum,frontallobeandvisualnetwork,whichishelpfultounderstandthe neuralmechanismsunderlyingFOGinPD.
ABSTRACT
Objective:To investigate dopaminergic neuron injury and ?-synuclein expression of mouse exposed chronically to low dose of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP). Methods:The C57BLmice received bake hypodermic injections of 25 mg/kg MPTP twice a week for 5 consecutive weeks. Abnormal behavior was observed during the treatment by using herbicide. The expression of throsine hydroxylase(TH)and ?-synuclein was determined by immunohistochemistry. The dopaminergic neurons apoptosis was determined by TdT-mediatd dUTP-biotin nick end labeling (TUNEL). Results:As compared with the controls of mice,those treated with MPTP displayed markedly hypoactive behavior. Immunohistochemical staining showed that the numbers of TH stain cells was decreased significantly after treatment with MPTP,and the density of ?-synuclein stain was increased significantly after treatment with MPTP. Apoptosis displayed after treatment with MPTP. Conclusion:Chronical injection with MPTP might induce abnormal behavior. apoptosis and continual aggregation of ?-synuclein in dopaminergic neurons of substantial nigra.