1.Efficiency of the occlusion therapy with and without levodopa-carbidopa in amblyopic children-A tertiary care centre experience.
Sofi IA1, Gupta SK2, Bharti A3, Tantry TG4. Int J Health Sci (Qassim). 2016 Apr;10(2):249-57.
OBJECTIVES: To assess the role, efficacy and tolerability of levodopa-carbidopa in the management of small and older children with different types of amblyopia.
2.Levodopa and neuropathy risk in patients with Parkinson disease: Effect of COMT inhibition.
Cossu G1, Ceravolo R2, Zibetti M3, Arca R4, Ricchi V4, Paribello A4, Murgia D4, Merola A3, Romagnolo A3, Nicoletti V2, Palermo G2, Mereu A5, Lopiano L3, Melis M4, Abbruzzese G6, Bonuccelli U2. Parkinsonism Relat Disord. 2016 Apr 20. pii: S1353-8020(16)30120-1. doi: 10.1016/j.parkreldis.2016.04.016. [Epub ahead of print]
OBJECTIVE: Our purpose was to determine whether the use of catechol-O-methyltransferase-inhibitors (ICOMT) can reduce the risk of developing levodopa (LD)-induced neuropathy in Parkinson's disease (PD) patients.
3.The single intake of levodopa modulates implicit learning in drug naïve, de novo patients with idiopathic Parkinson's disease.
Geffe S1, Schindlbeck KA1, Mehl A1, Jende J2, Klostermann F1, Marzinzik F3. J Neural Transm (Vienna). 2016 Apr 23. [Epub ahead of print]
Although dopamine is known to aggravate implicit learning, the exact impact on behaviour when feedback is unavailable remains unclear. Previous studies revealed that non-rewarded learning habits are affected in long-term dopaminergic treated patients with Parkinson's disease (PD). We studied the influence of a onetime levodopa intake on implicit learning in de novo, untreated PD patients. De novo PD patients (n = 22) before and after the single intake of levodopa and control subjects (n = 23) took part in a Go/NoGo paradigm. One stimulus was defined as target, which was first consistently preceded by one of three non-target stimuli (conditioning). This coupling was dissolved thereafter (deconditioning). In the 'Go version' subjects were asked to respond to the target by pressing a key, whereas in the 'NoGo version' response had to be inhibited. PD patients and controls (n = 14/n = 19) with an initial learning effect due to the target were included for further statistical analysis.
4.Levodopa-Induced Dyskinesia Is Related to Indirect Pathway Medium Spiny Neuron Excitotoxicity: A Hypothesis Based on an Unexpected Finding.
Ivanova SA1, Loonen AJ2. Parkinsons Dis. 2016;2016:6461907. doi: 10.1155/2016/6461907. Epub 2016 Apr 6.
A serendipitous pharmacogenetic finding links the vulnerability to developing levodopa-induced dyskinesia to the age of onset of Huntington's disease. Huntington's disease is caused by a polyglutamate expansion of the protein huntingtin. Aberrant huntingtin is less capable of binding to a member of membrane-associated guanylate kinase family (MAGUKs): postsynaptic density- (PSD-) 95. This leaves more PSD-95 available to stabilize NR2B subunit carrying NMDA receptors in the synaptic membrane. This results in increased excitotoxicity for which particularly striatal medium spiny neurons from the indirect extrapyramidal pathway are sensitive. In Parkinson's disease the sensitivity for excitotoxicity is related to increased oxidative stress due to genetically determined abnormal metabolism of dopamine or related products. This probably also increases the sensitivity of medium spiny neurons for exogenous levodopa. Particularly the combination of increased oxidative stress due to aberrant dopamine metabolism, increased vulnerability to NMDA induced excitotoxicity, and the particular sensitivity of indirect pathway medium spiny neurons for this excitotoxicity may explain the observed increased prevalence of levodopa-induced dyskinesia.
