Investigation of the Neuroprotective Efficacy of a Novel Therapeutic With Ashwagandha Root Extract and Ubisol-Q10 for Parkinson’s Disease

Iva Okaj, Caleb Vegh, Lauren Culmone, Darcy Wear, Rachel Huggard, Arpana Balachander, Sadia Almas, Sumeet Kaur, Siyaram Pandey Parkinson’s disease (PD), the second most prevalent neurodegenerative disease, is characterized by progressive loss of dopaminergic neurons in the substantia nigra pars compacta region of the brain. PD symptoms begin with a loss of movement coordination, including resting tremors, postural instability, bradykinesia and rigidity and progress to cognitive impairment, psychiatric irregularity, and death. While sporadic cases of PD are most common, paraquat (PQ) (a banned herbicide) exposure is another known cause. Although dopamine supplements and deep brain stimulation are available for symptomatic relief, there is no known preventative remedy for PD. This study is based on findings that Ubisol-Q10, a water-soluble formulation of coenzyme-Q10, shows unprecedented near-complete protection against oxidative stress-induced cell death. We have found that Ubisol-Q10 can neutralize mitochondrial dysfunction and exhibit neuroprotective effects in PQ exposed rats. Ethanolic root extract of ashwagandha (ASH) has also shown neuroprotective efficacy in maneb-paraquat treated mice. Our objective is to use a multidisciplinary approach to examine whether post-injury intervention with ASH along with Ubisol-Q10 can slow/halt the progression of neurodegeneration in a PQ-induced PD rat model. Our behavioural tests have shown that PQ-treated rats given Ubisol-Q10, ASH or a combination of both in drinking water have reduced motor impairment compared to rats given unsupplemented water. We have also found enhanced pro-survival astroglia activation in the treatment groups compared to negative controls. Treatment groups also showed a reduction in Iba-1 staining indicating lower levels of microglial (pro-inflammatory) activation. This research explores a novel therapeutic for Parkinson\u27s Disease with promising potential

Sodium-glucose co-transporter inhibitors and atrial fibrillation : A systematic review and meta-analysis of randomized controlled trials

BACKGROUND: Sodium-glucose co-transporter (SGLT) inhibitors reduce cardiovascular outcomes including mortality in several populations; however, their effect on atrial fibrillation/flutter (AF) remains unclear. Our objective was to determine whether SGLT inhibitors reduce AF and whether a history of AF modifies the effect of SGLT inhibitors on the composite of heart failure hospitalization or cardiovascular death. METHODS AND RESULTS: We searched MEDLINE, Embase, and CENTRAL to March 2021. Pairs of reviewers identified randomized controlled trials that compared an SGLT inhibitor with placebo or no therapy. We pooled data using RevMan 5.4.1, assessed risk of bias using the Cochrane tool, and determined the overall quality of evidence using Grades of Recommendation, Assessment, Development and Evaluation. Thirty-one eligible trials reported on AF events (75 279 participants, mean age 62 years, 35.0% women). Moderate quality evidence supported a lower risk of serious AF events with SGLT inhibitors (1.1% versus 1.5%; risk ratio 0.75 [95% CI, 0.66–0.86]; I2=0%). A similar reduction in total AF events was also noted with SGLT inhibitors. Three trials reported on heart failure hospitalization/cardiovascular death stratified by a baseline history of AF (18 832 participants, mean age 66 years, 38.1% women); in patients with a history of AF, SGLT inhibitors resulted in a lower risk in the composite of heart failure hospitalization or cardiovascular death (hazard ratio, 0.70 [95% CI, 0.57–0.85]; I2=0%)—similar to the effect estimate for patients without AF, P value for interaction: 1.00. CONCLUSIONS: SGLT inhibitors may reduce AF events and likely reduce heart failure hospitalization/cardiovascular death to a similar extent in patients with and without AF