Neural substrates and potential treatments for levodopa-induced dyskinesias in Parkinson's disease

Parkinson's disease (PD) is primarily a motor disorder that involves the gradual loss of motor function. Symptoms are observed initially in the extremities, such as hands and arms, while advanced stages of the disease can effect blinking, swallowing, speaking, and breathing. PD is a neurodegenerative disease, with dopaminergic neuronal loss occurring in the substantia nigra pars compacta, thus disrupting basal ganglia functions. This leads to downstream effects on other neurotransmitter systems such as glutamate, gamma-aminobutyric acid, and serotonin. To date, one of the main treatments for PD is levodopa. While it is generally very effective, prolonged treatments lead to levodopa-induced dyskinesia (LID). LID encompasses a family of symptoms ranging from uncontrolled repetitive movements to sustained muscle contractions. In many cases, the symptoms of LID can cause more grief than PD itself. The purpose of this review is to discuss the possible clinical features, cognitive correlates, neural substrates, as well as potential psychopharmacological and surgical (including nondopaminergic and deep brain stimulation) treatments of LID

FAM72D in plasma cell myeloma: a friend or enemy

Abstract Background Plasma cell neoplasm is characterized by complex genetic and prognostic heterogeneity. FAM72D, a gene located on chromosome 1, and the association between its expression and tumor progression and prognosis remain elusive. Methods The present study aims to assess FAM72D mRNA expression in 60 PCM patients and correlate its expression level with clinical and laboratory markers involved in diagnosing and prognosis of PCM using real-time PCR. Results Unpaired t-test revealed a significantly higher FAM72D expression level in the patients than in the control group with a median of 0.890 vs. /0.030, respectively, and p value = 0.000. The highest median level was denoted in newly diagnosed or relapsed patients (1.905, p value = 0.000). A significant positive correlation was found between FAM72D expression level and each of BMPCs count, M band, and β2 microglobulin (p = 0.000, p = 0.002, p = 0.024, respectively), and negative correlations with both serum albumin and hemoglobin level (p = 0.000, p = 0.035, respectively). The risk of relapse was 18.3-fold when the FAM72D level was greater than 1.547. Conclusion The higher FAM72D expression level in newly diagnosed and relapsed myeloma patients and its positive correlation with BMPCs confirm the stimulating effect of FAM72D on myeloma cell proliferation and its poor prognosis