Ubiquinol Supplementation Improves Gender-Dependent Cerebral Vasoreactivity and Ameliorates Chronic Inflammation and Endothelial Dysfunction in Patients with Mild Cognitive Impairment.

Ubiquinol can protect endothelial cells from multiple mechanisms that cause endothelial damage and vascular dysfunction, thus contributing to dementia. A total of 69 participants diagnosed with mild cognitive impairment (MCI) received either 200 mg/day ubiquinol (Ub) or placebo for 1 year. Cognitive assessment of patients was performed at baseline and after 1 year of follow-up. Patients' cerebral vasoreactivity was examined using transcranial Doppler sonography, and levels of Ub and lipopolysaccharide (LPS) in plasma samples were quantified. Cell viability and necrotic cell death were determined using the microvascular endothelial cell line bEnd3. Coenzyme Q10 (CoQ) levels increased in patients supplemented for 1 year with ubiquinol versus baseline and the placebo group, although higher levels were observed in male patients. The higher cCoQ concentration in male patients improved cerebral vasoreactivity CRV and reduced inflammation, although the effect of Ub supplementation on neurological improvement was negligible in this study. Furthermore, plasma from Ub-supplemented patients improved the viability of endothelial cells, although only in T2DM and hypertensive patients. This suggests that ubiquinol supplementation could be recommended to reach a concentration of 5 µg/mL in plasma in MCI patients as a complement to conventional treatment.

The duration of the motor response to apomorphine boluses is conditioned by the length of a prior infusion in Parkinson's disease.

"Pulsatile" administration of levodopa has been invocated a relevant factor for motor fluctuations in Parkinson's disease (PD). We studied dopaminergic sensitivity to apomorphine in 10 parkinsonian patients with motor fluctuations. Patients were tested as follows: the minimal effective dose of apomorphine (MED-1) was administered in the morning to induce an on response. Fifteen minutes after this motor response had disappeared, an apomorphine infusion was initiated and maintained to ensure on periods of three different durations on different days. Infusion lasted for approximately 30, 60 and 90 minutes. Subsequently, the infusion was stopped, and after 15 minutes in the off state, a second bolus of apomorphine (MED-2) was given. The mean infusion doses were 49.2 +/- 5.4, 108.4 +/- 10.3, and 150 +/- 8.2 mg. These elicited on periods of 48.2 +/- 4.1, 110 +/- 4.5, and 195 +/- 3.8 minutes. The MED-2 elicited on responses with a duration of 30 +/- 4.5, 18.4 +/- 3.2, and 11.2 +/- 4.1 minutes. The duration of the on response induced by the apomorphine infusions correlated inversely (P < 0.01) with the on induced by the MED-2 of apomorphine. Our findings indicate that a continuous dopaminergic stimulus may induce pharmacodynamic changes associated with tolerance in PD patients.

Parkinsonism Associated with Pathological 123I-FP-CIT SPECT (DaTSCAN) Results as the Initial Manifestation of Sporadic Creutzfeldt-Jakob Disease.

Sporadic Creutzfeldt-Jakob disease (sCJD) is a type of progressive, subacute encephalopathy associated with spongiform degeneration of the central nervous system. sCJD includes a broad and heterogeneous spectrum of clinical variants, but extrapyramidal symptoms and signs at disease onset were rarely reported. We describe a case of unilateral parkinsonism associated with pathological 123I-ioflupane SPECT (DaTSCAN) results as the initial manifestation of M129V subtype sCJD patient. To the best of our knowledge, only 2 cases of Creutzfeldt-Jakob disease demonstrating nigrostriatal dopaminergic deficits in vivo using DaTSCAN have been published in the literature.