INTRODUCTION: Coenzyme Q10, also known as Ubiquinone, is a substance now being used as a dietary supplement in many countries including the Philippines. It has also been the focus of several researches as treatment for several diseases including Parkinson's Disease. Several studies have shown that Coenzyme Q10 inhibits mitochondrial dysfunction in Parkinson's Disease, hence delaying its progression.
OBJECTIVES: The objective of this study is to assess and summarize the available evidence on the efficacy and safety of Coenzyme Q10 administration in the prevention of the progression of early Parkinson's Disease.
METHODS: This is meta-analysis of randomized controlled trials on the use of Coenzyme Q10 in Parkinson's Disease. A literature search in several databases was conducted for relevant studies. Three randomized controlled trials met the inclusion criteria. The efficacy of Coenzyme Q10 were measured using the total and the component scores of the Unified Parkinson Disease Rating Scale on follow-up. On the other hand, safety were measured using the withdrawal rate and the associated adverse reactions during the therapy of CoQ10. The Review Manager Software was utilized for the meta-analysis.
RESULTS: Compared to Placebo, treatment of CoQ10 did not show any significant difference in the mean scores of the UPDRS mental and ADL scores. Interestingly, the UPDRS motor score showed a significant difference between Coenzyme Q10 and placebo, but no significant difference when a subgroup analysis between high-dose (-4.03 [-15.07-7.01], p-value 0.47, I2 67%, P for heterogeneity 0.08) and low-dose Coenzyme Q10 (0.53 [-0.89-1.94], p-value 0.47, I2 34%, P for heterogeneity 0.22) was done. Overall, there was no significant difference in the total UPDRS score (0.68 [-0.61-1.97], p-value 0.30, I2 0%, P for heterogeneity 0.70). The anxiety, back pain, headache, sore throat, nausea, dizziness and constipation.
CONCLUSION: Contrary to some animal and human studies, this meta-analysis showed that the use of CoQ10 results to non-significant improvement in all components of the UPDRS scores as opposed to placebo. However, the use of CoQ10 is tolerated and seems to be safe but further studies are needed to validate this finding.

Neuroprotection ; Parkinson Disease

Background and Objectives. Neuroprotection agents may help improve the outcomes of large vessel ischemic stroke. This study aims to explore the role of Virgin Coconut Oil (VCO), with its well-documented anti-oxidant properties, in neuroprotection after transient occlusion of the extracranial internal carotid artery in a rat model of stroke. Methods. Twenty-three Sprague-Dawley rats were randomized into two groups: 1) control group (n=11) given distilled water, and 2) treatment group (n=12) given virgin coconut oil at 5.15 ml/kg body weight for seven days. Subsequently, the rats underwent transient right extracranial internal carotid artery occlusion (EICAO) for 5 minutes using non-traumatic aneurysm clips. At 4 and 24 hours after EICAO, the animals were examined for neurologic deficits by an observer blinded to treatment groups, then sacrificed. Eight brain specimens (4 from each group) were subjected to histopathologic examination (H & E staining) while the rest of the specimens were processed using triphenyltetrazolium chloride (TTC) staining to determine infarct size and area of hemispheric edema. Results. VCO treatment significantly improved the severity of neurologic deficit (1.42 ± 2.31) compared to the control distilled water group (4.09 ± 2.59) 24 hours after EICAO. Whereas, infarct size and percent hemispheric edema did not significantly differ between the two groups. Conclusion. Prophylactic treatment of VCO is protective against EICAO-induced neurologic deficits in a rat model. VCO shows great potential as a neuroprotective agent for large vessel ischemic stroke. However, more studies are necessary to elucidate the neuroprotective mechanisms of VCO therapy in ischemic stroke.
Coconut Oil ; Oxidants ; Antioxidants ; Neuroprotection ; Ischemia ; Stroke

Given the lack of infrastructure in Papua New Guinea (PNG) traumatic brain injury (TBI) cases are usually not retrieved quickly to medical centres. Cases that eventually reach the hospital do so after the golden hour has passed. This means that the brain is already at risk of or is already subject to secondary brain injury. In TBI, the parenchymal integrity of the normal, the penumbrous and the lacerated tissue needs to be kept in a state of balance, such that the normal tissue is not compromised. The whole aim of neuroprotection is to protect the normal brain parenchyma from further injury. Secondary brain injury is minimized by reducing cerebral oedema and intracranial pressure, in order to improve cerebral blood flow and perfusion. This guideline describes the options for neuroprotection in PNG.
Traumatic brain injuries ; Papua New Guinea ; neuroprotection ; Tissues ; Research

Ten seco-prezizaane sesquiterpenes were isolated from the water-soluble fraction of the fruit of Illicium lanceolatum using the combined methods of silica gel column chromatography,Sephadex LH-20 column chromatography,and RP-preparative HPLC. They were elucidated as majusanol E( 1),2α-hydroxycycloparviflorolide( 2),2β-hydroxy-3,6-dedioxypseudoanisatin( 3),majusanol A( 4),merrillianone( 5),cycloparvifloralone( 6),3α-hydroxycycloparvifloralone( 7),1,2-dehydrocycloparvifloralone( 8),henrylactone C( 9),and( 11) 7,14-ortholactone-3α-hydroxyfloridanolide( 10) according to the NMR data. All compounds were obtained from this plant for the first time. Neuroprotection activity,anti-Coxsackie B3 virus,and anti-H3 N2 virus experiments were carried out to test their bioactivities. The bioassay results showed that compounds 1,4,6,7,9 and 10 displayed weak protective effects of the damage of nerve SH-SY5 Y cell induced by monosodium glutamate.
Fruit ; Illicium ; Magnetic Resonance Spectroscopy ; Molecular Structure ; Neuroprotection ; Sesquiterpenes

Stroke is one of the leading causes of death and physical disability worldwide. The consequences of stroke injuries are profound and persistent, causing in considerable burden to both the individual patient and society. Current treatments for ischemic stroke injuries have proved inadequate, partly owing to an incomplete understanding of the cellular and molecular changes that occur following ischemic stroke. MicroRNAs (miRNA) are endogenously expressed RNA molecules that function to inhibit mRNA translation and have key roles in the pathophysiological processes contributing to ischemic stroke injuries. Potential therapeutic areas to compensate these pathogenic processes include promoting angiogenesis, neurogenesis and neuroprotection. Several miRNAs, and their target genes, are recognized to be involved in these recoveries and repair mechanisms. The capacity of miRNAs to simultaneously regulate several target genes underlies their unique importance in ischemic stroke therapeutics. In this Review, we focus on the role of miRNAs as potential diagnostic and prognostic biomarkers, as well as promising therapeutic agents in cerebral ischemic stroke.
Biomarkers ; Cause of Death ; Humans ; Ischemia ; MicroRNAs* ; Neurogenesis ; Neuroprotection ; Protein Biosynthesis ; RNA ; Stroke*

Cyperi Rhizoma (CR), the rhizome of Cyperus rotundus L., exhibits neuroprotective effects in in vitro and in vivo models of neuronal diseases. Nevertheless, no study has aimed at finding the neuroactive constituent(s) of CR. In this study, we identified active compounds in a CR extract (CRE) using bioactivity-guided fractionation. We first compared the anti-oxidative and neuroprotective activities of four fractions and the CRE total extract. Only the ethyl acetate (EA) fraction revealed strong activity, and further isolation from the bioactive EA fraction yielded nine constituents: scirpusin A (1), scirpusin B (2), luteolin (3), 6′-acetyl-3,6-diferuloylsucrose (4), 4′,6′ diacetyl-3,6-diferuloylsucrose (5), p-coumaric acid (6), ferulic acid (7), pinellic acid (8), and fulgidic acid (9). The activities of constituents 1-9 were assessed in terms of anti-oxidative, neuroprotective, anti-inflammatory, and anti-amyloid-β activities. Constituents 1, 2, and 3 exhibited strong activities; constituents 1 and 2 were characterized for the first time in this study. These results provide evidence for the value of CRE as a source of multi-functional neuroprotectants, and constituents 1 and 2 may represent new candidates for further development in therapeutic use against neurodegenerative diseases.
Cyperus ; In Vitro Techniques ; Luteolin ; Neurodegenerative Diseases ; Neurons ; Neuroprotection ; Neuroprotective Agents ; Rhizome

OBJECTIVES: The effects of serum uric acid (UA) level on a variety of diseases were found from experimental and observational studies via oxidative stress and anti-oxidants. However, research on the association of UA and hearing thresholds is relatively sparse. We investigated this issue in the U.S. general population to evaluate the relationship of serum UA levels and pure tone threshold of hearing. METHODS: Forty four thousand eighty four eligible participants aged 20 to 69 years who have serum UA data and received Audiometry Examination Component were enrolled from the National Health and Nutrition Examination Survey 1999–2004. Hearing thresholds (dB) as a pure tone average at low frequencies (0.5, 1, 2 kHz) and at high frequencies (3, 4, 6, and 8 kHz) were computed. Multivariate linear regression models and tertile-based analysis with an extended-model approach for covariates adjustment were used to assess the correlation between serum UA level and hearing thresholds. RESULTS: In the adjusted mode of tertile-based analysis, the regression coefficients elucidated as the change of log-transformed mean hearing thresholds upon comparing participants in the highest tertile of serum UA to those in the lowest tertile were –0.067 (P=0.023) in high frequency and –0.058 (P=0.054) in low frequency. After adjusting for multiple pertinent covariates, inverse association between tertiles of serum UA and hearing thresholds remained essentially unchanged. The negative trends between serum UA and hearing thresholds were statistically significant (P for trends <0.05) in tertile-based multiple linear regressions. CONCLUSION: Individuals with elevated UA levels independently were found to be inversely associated with hearing thresholds for pure tone audiometry in a nationally representative sample of U.S. adults.
Adult ; Antioxidants ; Audiometry ; Hearing* ; Humans ; Linear Models ; Neuroprotection ; Nutrition Surveys ; Oxidative Stress ; Uric Acid*

Protons are widespread in cells and serve a variety of important functions. In certain pathological conditions, acid-base balance was disrupted and therefore excessive protons were generated and accumulated, which is termed acidosis and proved toxic to the organism. In the nervous system, it has been reported that acidosis was a common phenomenon and contributed to neuronal injury in various kinds of neurological diseases, such as ischemic stroke, multiple sclerosis and Huntington's disease. Acid-sensing ion channels (ASICs) is the key receptor of protons and mediates acidosis-induced neuronal injury, but the underlying mechanism remains unclear. Traditionally, Ca(2+) influx through homomeric ASIC1a channels has been considered to be the main cause of acidotoxicity. Recent research showed that extracellular protons trigger a novel form of necroptosis in neurons via ASIC1a-mediated serine/threonine kinase receptor interaction protein 1 (RIP1) activation, independent of ion-conducting function of ASIC1a. In addition, ASIC1a was found in mitochondria and regulated mitochondrial permeability transition-dependent neuronal death. In this article, we will review the recent progresses on the mechanisms underlying ASIC-mediated neuronal death and discuss ASIC modulators involved in this process.
Acid Sensing Ion Channels ; Acid-Base Equilibrium ; Acidosis ; Cell Death ; Neurons ; Neuroprotection

Presently, treatment of PD focuses on symptomatic therapy, that is to control motor symptoms, at the lowest possible dose, so as nor to develop early drug resistance, and consequent extrapyramidal symtoms. However, there has been no clinical trial, to date that has provided definitive evidence of pharmacological neuroprotection. Among the drugs with possible neuroprotective effects are the dopamine agonists.
OBJECTIVE: The objective of this study is to determine the efficacy and safety of Rotigotine transdermal patch in the treatment of early Parkinson's disease in terms of improvement in the functional capacity and the incidence of adverse effects in patients treatment with the said drug .
METHODOLOGY: Literature search of all randomized controlled trials, published from 1999-2009 comparing rotigotine patch with placebo, in patients with Parkinson's disease. Types of outcome measures- The primary outcome studied was the number of responders described as those with> 20% decrease in UPDRS Scores. The secondary outcome include the mean change in UPDRS score and the total incidence of adverse effects on patients on rotigotine patch.
RESULTS: The use of Rotigotine patch in early Parkinson's disease shows as trend toward benefit and was statistically significant (OR 0.33) in terms of number of patients who showed a significant change in UPRDS scores. In terms of UPDRS scoring, there was significant improvement for those who took Rotigotene (MD 5.2.5). However, incidence of adverse effects was higher in the Rotigotine group compared to the placebo group (OR 3.13)
CONCLUSION: The evidence from this review supports the use of Rorigotine patch for the treatment of early Parkinson's disease. This has shown to produce clinical improvement in parkinsonian symptoms as measured by the significant decrease in the UPDRS Scores on follow-up. However, adverse events were similar to those found with other dopamine agonists.

Human ; Dopamine Agonists ; Drug Resistance ; Neuroprotection ; Neuroprotective Agents ; Parkinson Disease ; Parkinsonian Disorders ; Tetrahydronaphthalenes ; Thiophenes ; Transdermal Patch

For decades, numerous pharmacological and non-pharmacological strategies have been evaluated without success to limit the consequences of the ischemic cascade, but more rarely the therapies were explored as add on remedies on individuals also receiving reperfusion therapies. It is plausible that these putative neuroprotectants never reached the ischemic brain in adequate concentrations. Currently, the concept of neuroprotection incorporates cerebral perfusion as an obligatory substrate upon which ischemic brain survival depends, and it is plausible that some of the compounds tested in previous neuroprotection trials might have resulted in more favorable results if reperfusion therapies had been co-administered. Nonetheless, pharmacological or mechanical thrombectomy are frequently powerless to fully reperfuse the ischemic brain despite achieving a high rate of recanalization. This review covers in some detail the importance of the microcirculation, and the barriers that may hamper flow reperfusion at the microcirculatory level. It describes the main mechanisms leading to microcirculatory thrombosis including oxidative/nitrosative stress and refers to recent efforts to ameliorate brain perfusion in combination with the co-administration of neuroprotectants mainly aimed at harnessing oxidative/nitrosative brain damage.
Antioxidants ; Brain ; Microcirculation ; Neuroprotection ; Neuroprotective Agents* ; Oxidative Stress ; Perfusion ; Reperfusion* ; Stroke ; Thrombectomy ; Thrombosis