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.

Gastrodin is the main bioactive component of Gastrodia elata Blume (G. elata). Tian Ma Su Zhu She Ye (contains Gastrodin) It is an extensively used in the clinical practice of traditional Chinese medicine, to treat neurasthenia, neurasthenia syndrome, angioneurotic headache disorder, traumatic brain syndrome, vertigo meniere disease, medicinal with dizziness, vertigo, sudden deafness, vestibular neuronitis, vertebral basilar artery blood supply deficiency, etc. Apart from traditional claims, scientific reports support the antioxidative, anticonvulsive, antiinflammatory, antiepileptic, antiobesity, anxiolytic, and learning and memory improvements in activities of gastrodin

Roxindole (EMD-49,980) is a dopaminergic and serotonergic drug which was originally developed for the treatment of schizophrenia. Roxindole has also been investigated as a therapy for the major depressive disorder, Parkinson's disease, and prolactinoma. Roxindole is dopamine autoreceptor-selective agonistic drug with high affinity to D2-like receptors and with much lower affinities to D1-like, % and ol2, muscarinic and 5HT 2 receptors. Additionally, Roxindole exerts 5HT uptake inhibition and 5HT1A agonistic effects. The bioavailability of Roxindole has been estimated at 5% due to a high first-pass metabolization. On the other hand, in 14C distribution studies, Roxindole has crossed the blood-brain barrier readily and the brain concentrations at all intervals have been much higher than corresponding plasma levels. In clinical trials, Roxindole ‘s antipsychotic efficacy was only modest but it was unexpectedly found to produce potent and rapid antidepressant and anxiolytic effects. However, the clinical development of Roxindole was discontinued.

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.

Budipine is an antiparkinsonian drug, which was developed by Byk Gulden (now Takeda) for the treatment of Parkinson's disease. The drug has multiple mechanisms of action: it was found to interfere with dopamine biosynthesis, mainly by inhibiting MAO-B enzyme and stimulating aromatic L-amino acid decarboxylase. Also the drug inhibits the dopamine re-uptake and has weak affinity to NMDA and muscarinic receptors. Budipine passes the blood-brain barrier, is metabolized by hydroxylation, and is excreted by both in urine and feces within 24 h.

Piribedil is an antiparkinsonian agent which acts as D2 and D3 receptor agonist. In European countries and worldwide it is used as a monotherapy or in combination with dopatherapy for treatment of Parkinson's disease, cognitive impairment and obliterating arteriopathy.

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.

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.

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.

Piroheptine is an antagonist of muscarinic acetylcholine receptors. The drug was used for the treatment of Parkinson's disease, however, it is no longer marketed.