Latest Research News on Parkinson’s Disease: Nov – 2019

Parkinson’s Disease

Pathophysiology The institution of a model of paralysis agitans through the administration of MPTP to apelike primates has provided vital insights into new therapeutic methods. A typical parkinsonian syndrome develops within the animals that’s characterised by dopaminergic-cell loss within the locus niger and putting abnormalities within the spontaneous activity and bodily function responses of neurons within the basal ganglia.94,95 A elementary discovery has been that the dopamine-deficiency state is related to augmented activity of the restrictive γ-aminobutyric acid (GABA)–employing (GABAergic) output nuclei within the basal ganglia, the inner phase of the paleostriatum, and also the pars reticulata of the substantia. [1]

Epidemiology of Parkinson’s disease

The causes of Parkinson’s sickness (PD), the second commonest neurodegenerative disorder, are still mostly unknown. Current thinking is that major factor mutations cause solely atiny low proportion of all cases which in most cases, non-genetic factors play a region, most likely in interaction with condition genes. varied epidemiologic studies are done to spot such non-genetic risk factors, however most were little and methodologically restricted. Larger, well-designed prospective cohort studies have solely recently reached a stage at that they need enough incident patients and person-years of follow-up to research attainable risk factors and their interactions. during this article, we tend to review what’s better-known concerning the prevalence, incidence, risk factors, and prognosis of atomic number 46 from epidemiologic studies. [2]

The ubiquitin pathway in Parkinson’s disease

Mutations of the α-synuclein gene1,2 are known in some familial sorts of Parkinson’s disease, and α-synuclein macromolecule has been shown to accumulate within the brains of patients with the disease3. These findings counsel that Parkinson’s disease is also caused by the abnormal aggregation of α-synuclein macromolecule. Here we’ve got known during a German family with Parkinson’s disease a missense mutation within the ubiquitin carboxy-terminal hydrolase L1 (UCH-L1) sequence. we tend to show that this mutation, Ile93Met, causes a partial loss of the chemical action activity of this thiol peptidase, that may lead to aberrations within the chemical process pathway and aggregation of proteins. [3]

Cav2.3 channels contribute to dopaminergic neuron loss in a model of Parkinson’s disease

Degeneration of dopaminergic neurons within the neural structure causes the motor symptoms of Parkinson’s malady. The mechanisms underlying this age-dependent and region-selective neurodegeneration stay unclear. Here we tend to establish Cav2.3 channels as regulators of nigral somatic cell viability. Cav2.3 transcripts were additional torrential than alternative voltage-gated Ca2+ channels in mouse nigral neurons and upregulated throughout aging. Plasmalemmal Cav2.3 supermolecule was over in dopaminergic neurons of the ventral tegmental space, that don’t degenerate in Parkinson’s malady. Cav2.3 knockout reduced activity-associated nigral corporeal Ca2+ signals and Ca2+-dependent after-hyperpolarizations, and afforded full protection from degeneration in vivo during a toxin Parkinson’s mouse model. [4]

Analysis of Motor Complications in Parkinson’s Disease Phenotypes

Patients with metal were registered within the analysis study and underwent examination on movement disorder and drug-induced motor complication by UPDRS III and IV. Hoehn and Yahr scale was wont to describe the intermediate course of illness. All antiparkinsonian medicine were calculated on theoretical equivalence to dihydroxyphenylalanine. 208 patients were divided into 3 subgroups: tremor-dominant fifty,4%, akinetic-rigid forty one,9% and blend sort seven,7%. All patients were treated with dihydroxyphenylalanine, and concerning 3 quarters were together with a Intropin agonist.Regarding illness period and developing of carrying off, there was vital distinction per clinical makeup. AR and blend subtype of metal develop carrying off earlier among three years compare to TD. 72,4% TD sort develop carrying off once half dozen years and additional whereas AR and blend sort develop earlier. [5]


[1] Lang, A.E. and Lozano, A.M., 1998. Parkinson’s disease. New England Journal of Medicine, 339(16), (Web Link)

[2] De Lau, L.M. and Breteler, M.M., 2006. Epidemiology of Parkinson’s disease. The Lancet Neurology, 5(6), (Web Link)

[3] Leroy, E., Boyer, R., Auburger, G., Leube, B., Ulm, G., Mezey, E., Harta, G., Brownstein, M.J., Jonnalagada, S., Chernova, T. and Dehejia, A., 1998. The ubiquitin pathway in Parkinson’s disease. Nature, 395(6701), (Web Link)

[4] Cav2.3 channels contribute to dopaminergic neuron loss in a model of Parkinson’s disease
Julia Benkert, Simon Hess, […]Birgit Liss
Nature Communications volume 10, Article number: 5094 (2019) (Web Link)

[5] Mansurova, N. and Dildora, Q. (2018) “Analysis of Motor Complications in Parkinson’s Disease Phenotypes”, Journal of Advances in Medicine and Medical Research, 25(5), (Web Link)