Coenzyme Q10, also known as ubiquinone, ubidecarenone, coenzyme Q, and abbreviated at times to CoQ10 or Q10 is a coenzyme that is ubiquitous in the bodies of most animals. It is a 1,4-benzoquinone, where Q refers to the quinone chemical group and 10 refers to the number of isoprenyl chemical subunits in its tail. This fat-soluble substance, which resembles a vitamin, is present in most eukaryotic cells, primarily in the mitochondria. It is a component of the electron transport chain and participates in aerobic cellular respiration, which generates energy in the form of ATP. Ninety-five percent of the human body’s energy is generated this way. Therefore, those organs with the highest energy requirements—such as the heart, liver, and kidney—have the highest CoQ10 concentrations. There are three redox states of CoQ10: fully oxidized (ubiquinone), semiquinone (ubisemiquinone), and fully reduced (ubiquinol). The capacity of this molecule to act as a 2 electron carrier (moving between the quinone and quinol form) and 1 electron carrier (moving between the semiquinone and one of these other forms) is central to its role in the electron transport chain, and as radical-scavenging antioxidant. Coenzyme Q10 works foremost in every cell of your body to synthesize energy. In cells' mitochondria, CoQ10 helps generate adenosine triphosphate (ATP), your body's energy currency. It makes sense that organs with the highest energy needs - including the heart, liver, and kidneys - contain large amounts of CoQ10. Among its roles, ubiquinol protects fats, protein, low-density lipoprotein (LDL, a cholesterol transporter), and DNA from oxidative damage. It also regenerates vitamin E, another powerful antioxidant. Even though Coenzyme Q10 is a supplement and occurs naturally in your body, it doesn't mean that it's side effect free. However, most CoQ10 side effects are mild. Some people may experience allergies to increased Coenzyme Q10. There have been some reports of rashes and itching. Other side effects include a lowering of blood sugar within the body. CoQ10 is not approved by the U.S. Food and Drug Administration (FDA) for the treatment of any medical condition. It is sold as a dietary supplement. In the U.S., supplements are not regulated as drugs, but as foods. How CoQ10 is manufactured is not regulated and different batches and brands may vary significantly. As an over-the-counter nutritional supplement, CoQ10 has been used to treat many things, from heart disease, high blood pressure and high cholesterol to diabetes, breast cancer and gum disease. CoQ10 supposedly can help with immune deficiencies, increase fertility, treat Alzheimer's and Parkinson's, reduce ringing in the ears, delay aging and improve skin, and increase athleticism The key benefits of coenzyme Q10 are summarized as below. A 2014 Cochrane Collaboration meta-analysis found "no convincing evidence to support or refute" the use of CoQ10 for the treatment of heart failure. Evidence with respect to preventing heart disease in those who are otherwise healthy is also poor. A 2009 Cochrane review concluded that studies looking at the effects of CoQ10 on blood pressure were unreliable, and therefore no conclusions could be made regarding its effectiveness in lowering blood pressure. Available evidence suggests that "CoQ10 is likely ineffective in moderately improving" the chorea associated with Huntington's disease. No large well-designed clinical trials of CoQ10 in cancer treatment have been done. The National Cancer Institute identified issues with the few, small studies that have been done stating, "the way the studies were done and the amount of information reported made it unclear if benefits were caused by the CoQ10 or by something else". The American Cancer Society has concluded, "CoQ10 may reduce the effectiveness of chemo and radiation therapy, so most oncologists would recommend avoiding it during cancer treatment. Lower levels of CoQ10 have also been observed in people with Parkinson's disease. Preliminary research has found that increasing CoQ10 may increase levels of the neurotransmitter dopamine, which is thought to be lowered in people with Parkinson's disease. It has also been suggested that CoQ10 might protect brain cells from damage by free radicals. A small, randomized controlled trial examined the use of 360 mg CoQ10 or a placebo in 28 treated and stable Parkinson's disease patients. After 4 weeks, CoQ10 provided a mild but significant significant mild improvement in early Parkinson's symptoms and significantly improved performance in visual function. As an antioxidant, Coenzyme Q10 helps protect your body against the harmful effects of toxins and also aids the absorption of beneficial vitamins and minerals. Antioxidants are sometimes credited with boosting weight loss, possibly due to their energising effect on the body helping increase the fat-burning benefits of exercise.

Benserazide is a peripherally-acting aromatic L-amino acid decarboxylase (AADC) or DOPA decarboxylase inhibitor. Benserazide is only used in conjunction with L-dopa for the treatment of Parkinson's disease under the brand name Madopar in the UK. Madopar HBS (125 mg) is a controlled-release dosage form with 100 mg L-dopa and 25 mg benserazide.

Lazabemide is a reversible and selective inhibitor of monoamine oxidase B (MAO-B) that was under clinical development against Parkinson's disease, Alzheimer's disease and as an aid to smoking cessation. The development of the drug was discontinued due to liver toxicity.

Ginsenoside B2 is a constituent of Panax ginseng (ginseng) and Panax japonicum (Japanese ginseng). Ginsenoside B2 belongs to the family of Triterpene Glycosides. Many reports demonstrated that Ginsenoside B2 possesses the multifaceted beneficial pharmacological effects on cardiovascular system. Ginsenoside B2 has negative effect on cardiac contractility and autorhythmicity. It causes alternations in cardiac electrophysiological properties, which may account for its antiarrhythmic effect. In addition, Ginsenoside B2 also exerts antiischemic effect and induces angiogenic regeneration. Ginsenoside B2 is an extract from Panax notoginseng, which is a well-known traditional Chinese medicine that has been used for the treatment of various diseases for years. Ginsenoside B2 has been reported to decrease Aβ in Alzheimer's disease animal models. Ginsenoside B2 is a component of Korean Red Ginseng. The ginsenoside content of the red ginseng is shown as Rg1: 3.3 mg/g, Re (B2): 2.0 mg/g, Rb1: 5.8 mg/g, Rc: 1.7 mg/g, Rb2: 2.3 mg/g, and Rd: 0.4 mg/g, respectively. Korean ginseng (Panax ginseng Meyer, Araliaceae) is traditionally used as an important herbal medicine in Far East Asia. Korean Red Ginseng is possibly effective for: • Alzheimer's disease. Evidence shows that taking Panax ginseng root daily for 12 weeks can improve mental performance in people with Alzheimer's disease. • Lung disease called chronic obstructive pulmonary disease (COPD). Taking Panax ginseng by mouth seems to improve lung function and some symptoms of COPD. • Mental function. Taking Panax ginseng by mouth might improve abstract thinking, mental arithmetic skills, and reaction times in healthy, middle-aged people but not in young adults. Panax ginseng alone does not seem to improve memory. But there is some evidence that a combination of Panax ginseng and ginkgo leaf extract can improve memory in otherwise healthy people between the ages of 38 and 66. • Erectile dysfunction (ED). Taking Panax ginseng by mouth seems to improve sexual function in men with erectile dysfunction. • Flu. Taking a specific Panax ginseng by mouth appears to reduce the risk of getting a cold or the flu. But, taking Panax ginseng does not seem to reduce flu symptoms or the length of the illness. • Multiple sclerosis-related fatigue. Taking Panax ginseng daily for 3 months reduces feelings of tiredness and improves quality of life in females with MS. • Premature ejaculation. Applying a cream containing Panax ginseng, angelica root, Cistanches deserticola, Zanthoxyl species, torlidis seed, clover flower, asiasari root, cinnamon bark, and toad venom (SS Cream) to the penis one hour before intercourse and washing off immediately before intercourse seems to help prevent premature ejaculation. • Sexual arousal. Taking powdered Korean red ginseng, a specific form of Panax ginseng, seems to improve sexual arousal and satisfaction in postmenopausal women.

18F-beta-CIT-FP is a cocaine analog with high affinity for the dopamine transporter. The compound is used as an imaging agent for PET studies and was approved in Korea to diagnose Parkinson's disease.

Talipexole is a D2 receptor agonist which was marketed in June 1996 in Japan for the treatment of Parkinson's disease. Clinical trials with talipexole in patients with Parkinson's disease demonstrated statistically significant improvements from baseline for parkinsonian symptoms including akinesia, rigidity, tremor and gait disturbances.

Entacapone is a selective and reversible inhibitor of catechol-O-methyltransferase (COMT), that in combination with carbidopa and levodopa used for the treatment of Parkinson's disease. Physiological substrates of COMT include DOPA, catecholamines (dopamine, norepinephrine, and epinephrine) and their hydroxylated metabolites. The function of COMT is the elimination of biologically active catechols and some other hydroxylated metabolites. When decarboxylation of levodopa is prevented by carbidopa, COMT becomes the major metabolizing enzyme for levodopa, catalyzing its metabolism to 3-methoxy-4-hydroxy-L-phenylalanine (3-OMD). When entacapone is given in conjunction with levodopa and carbidopa, plasma levels of levodopa are greater and more sustained than after administration of levodopa and carbidopa alone. It is believed that at a given frequency of levodopa administration, these more sustained plasma levels of levodopa result in more constant dopaminergic stimulation in the brain, leading to greater effects on the signs and symptoms of Parkinson’s disease. The higher levodopa levels may also lead to increased levodopa adverse effects, sometimes requiring a decrease in the dose of levodopa. When 200 mg entacapone is coadministered with levodopa/carbidopa, it increases levodopa plasma exposure (AUC) by 35-40% and prolongs its elimination half-life in Parkinson’s disease patients from 1.3 to 2.4 hours. Plasma levels of the major COMT-mediated dopamine metabolite, 3-methoxy-4-hydroxy-L-phenylalanine (3-OMD), are also markedly decreased proportionally with increasing dose of entacapone. In animals, while entacapone enters the CNS to a minimal extent, it has been shown to inhibit central COMT activity. In humans, entacapone inhibits the COMT enzyme in peripheral tissues. The effects of entacapone on central COMT activity in humans have not been studied.

Raclopride is a salicylamide neuroleptic, that acts as a selective antagonist of D2 dopamine receptors both in vitro and in vivo. Tritium-labelled raclopride has properties that demonstrate its usefulness as a radioligand for the labelling of dopamine-D2 receptors : 3H-Raclopride has a high affinity for the rat and human dopamine-D2 receptors, the non-specific binding of 3H-raclopride is very low, not exceeding 5% of the total binding and the distribution of the 3H-raclopride binding sites in the brain closely correlates with the dopaminergic innervation. The binding of 3H-raclopride is blocked by dopamine-D2 agonists and antagonists, while the D1 agonist SKF 38393 and the Dl antagonist SCH 23390 have much less potency. The interaction of dopamine with 3H-raclopride binding results in a shallow competition curve, which suggests that 3H-raclopride, similar to other dopamine-D2 radioligands, labels both high and low agonist affinity states of the dopamine-D2 receptor. The in vivo receptor binding studies performed with 3H-raclopride also demonstrate its favorable properties as a dopamine-D2 receptor marker in vivo In contrast to some other compounds used as radioligands, raclopride enters the brain readily and binds with a low component of non-specific binding in all dopamine-rich brain areas. A saturation curve may be achieved in vivo binding studies since injections of increasing concentrations of 3H-raclopride appears to be saturated at concentrations above 25 mkCi (corresponding to approximately 5 nmol/kg). Raclopride antagonizes apomorphine-induced hyperactivity in the rat at low doses (ED50 = 130 nM/kg i.p.) but induces catalepsy only at much higher doses (ED50 = 27 mkM/kg i.p.). Radiolabelled raclopride has been used as a ligand for in vitro and in vivo autoradiography in rat and primate brains. Raclopride C 11 is used with positron emission tomography (PET) as a clinical research tool to determine dopamine type 2 (D 2) receptor density in the human brain under normal and pathological conditions. For example, raclopride C 11 used in PET studies has served to confirm the age-related decrease in striatal dopamine D2 receptor density, which may be associated with a decline in the motor as well as cognitive functions. In patients with Alzheimer's disease, raclopride C 11 may be used to examine neuroreceptor distribution and quantities, which may help in the analysis of degenerative alterations of neuron populations and neuroreceptor systems in patients with this disease. In Huntington's disease, in which degeneration of neostriatal interneurons occurs (postsynaptic to the dopaminergic input), specific binding of raclopride C 11 to D 2 receptors may serve as one of the parameters in predicting performance in cognitive tasks.

Kavain is the main kavalactone found mostly in the roots of the kava plant. Kavain interacts with voltage-dependent Na+ and Ca2+ channels, GABAA ion channels. Kavain is found to be involved in TNF-alpha expression in human and mouse cells via regulation transcriptional factors. Kavain exhibits neuroprotective effects in models of Alzheimer's and Parkinson's diseases, and produces anxyolitic effect.

Oleoylethanolamide (oleic monoethanolamide, OEA), the naturally occurring amide of ethanolamine and oleic acid, is an endogenous lipid that modulates feeding, body weight, and lipid metabolism by binding with high affinity to the ligand-activated transcription factor, peroxisome proliferator-activated receptor-alpha (PPAR-alpha). OEA reveals the pharmacological properties in the treatment of obesity, atherosclerosis and other diseases. It was shown, that OEA can be used to control hunger in Prader-Willi syndrome, in addition, it exhibited neuroprotective properties in Parkinson's disease experiments. OEA is an endogenous ligand of the orphan receptor GPR119, a G protein-coupled receptor (GPCR) expressed predominantly in the human and rodent pancreas and gastrointestinal tract and in rodent brain, suggesting that the reported effects of OEA on food intake may be mediated, at least in part, via the GPR119 receptor. Recently was shown, that OEA was an effective inhibitor of hyperpigmentation through activation of ERK, Akt and p38 pathways, inhibition of the CREB pathway, and subsequent down-regulation of MITF, TRP-1 and tyrosinase production. Therefore, OEA could be a useful therapeutic agent for use in the treatment of hyperpigmentation and could be an effective component in whitening and lightening cosmetics.