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Total 422235 Results
| Label | Description | ILX | Version | Created CID | Modified Time | ||||||
|---|---|---|---|---|---|---|---|---|---|---|---|
| GABRB3 | taken from OMIM | ILX:0104518 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| GAD67 | An enzyme that catalyzes the production of gamma-aminobutyric acid from L-glutamic acid. | ILX:0104519 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Gadobenate Dimeglumine | In magnetic resonance imaging (MRI), visualization of normal and pathological brain tissue depends in part on variations in the radiofrequency signal intensity that occur with changes in proton density, alteration of the T1, and variation in the T2. When placed in a magnetic field, Gadobenate Dimeglumine shortens both the T1 and the T2 relaxation times in tissues where it accumulates. At clinical doses, Gadobenate Dimeglumine primarily affects the T1 relaxation time, thus producing an increase in signal intensity. Gadobenate Dimeglumine does not cross the intact blood-brain barrier; therefore, it does not accumulate in normal brain tissue or in central nervous system (CNS) lesions that have not caused an abnormal blood-brain barrier (e.g., cysts, mature post-operative scars). Pharmacology: Gadobenate dimeglumine shares the pharmacokinetic properties of the ECF contrast agent gadopentetate dimeglumine; however, gadobenate differs in that is also selectively taken-up by hepatocytes and excreted via the bile (up to 5% of dose). The elimination half-life of gadobenate dimeglumine is approximately 1 hour. It is not metabolized. Mechanism of action: Based on the behavior of protons when placed in a strong magnetic field, which is interpreted and transformed into images by magnetic resonance (MR) instruments. Paramagnetic agents have unpaired electrons that generate a magnetic field about 700 times larger than the proton's field, thus disturbing the proton's local magnetic field. When the local magnetic field around a proton is disturbed, its relaxation process is altered. MR images are based on proton density and proton relaxation dynamics. MR instruments can record 2 different relaxation processes, the T1 (spin-lattice or longitudinal relaxation time) and the T2 (spin-spin or transverse relaxation time). In magnetic resonance imaging (MRI), visualization of normal and pathological brain tissue depends in part on variations in the radiofrequency signal intensity that occur with changes in proton density, alteration of the T1, and variation in the T2. When placed in a magnetic field, Gadobenate Dimeglumine shortens both the T1 and the T2 relaxation times in tissues where it accumulates. At clinical doses, Gadobenate Dimeglumine primarily affects the T1 relaxation time, thus producing an increase in signal intensity. Gadobenate Dimeglumine does not cross the intact blood-brain barrier; therefore, it does not accumulate in normal brain tissue or in central nervous system (CNS) lesions that have not caused an abnormal blood-brain barrier (e.g., cysts, mature post-operative scars). Drug type: Approved. Small Molecule. Drug category: Contrast Media | ILX:0104520 | 4 | FDI Lab - SciCrunch.org | 08/24/2018 | FDI Lab - SciCrunch.org | term | 12/08/2016 | 0 | NeuroLex | troy sincomb |
| Gadodiamide | Gadodiamide is a gadolinium based contrast agent used in MR imaging procedures to assist in the visualization of blood vessels. It is commonly marketed under the trade name Omniscan. (Wikipedia) Pharmacology: Not Available Mechanism of action: Based on the behavior of protons when placed in a strong magnetic field, which is interpreted and transformed into images by magnetic resonance (MR) instruments. Paramagnetic agents have unpaired electrons that generate a magnetic field about 700 times larger than the proton's field, thus disturbing the proton's local magnetic field. When the local magnetic field around a proton is disturbed, its relaxation process is altered. MR images are based on proton density and proton relaxation dynamics. MR instruments can record 2 different relaxation processes, the T1 (spin-lattice or longitudinal relaxation time) and the T2 (spin-spin or transverse relaxation time). In magnetic resonance imaging (MRI), visualization of normal and pathological brain tissue depends in part on variations in the radiofrequency signal intensity that occur with changes in proton density, alteration of the T1, and variation in the T2. When placed in a magnetic field, gadodiamide shortens both the T1 and the T2 relaxation times in tissues where it accumulates. At clinical doses, gadodiamide primarily affects the T1 relaxation time, thus producing an increase in signal intensity. Gadodiamide does not cross the intact blood-brain barrier; therefore, it does not accumulate in normal brain tissue or in central nervous system (CNS) lesions that have not caused an abnormal blood-brain barrier (e.g., cysts, mature post-operative scars). Abnormal vascularity or disruption of the blood-brain barrier allows accumulation of gadodiamide in lesions such as neoplasms, abscesses, and subacute infarcts. Drug type: Approved. Small Molecule. Drug category: Contrast Media | ILX:0104521 | 4 | FDI Lab - SciCrunch.org | 08/24/2018 | FDI Lab - SciCrunch.org | term | 12/08/2016 | 0 | NeuroLex | troy sincomb |
| Gadopentetate dimeglumine | A complex of gadolinium with a chelating agent, diethylenetriamine penta-acetic acid (DTPA see pentetic acid), that is given to enhance the image in cranial and spinal MRIs. (From Martindale, The Extra Pharmacopoeia, 30th ed, p706) Pharmacology: Not Available Mechanism of action: Based on the behavior of protons when placed in a strong magnetic field, which is interpreted and transformed into images by magnetic resonance (MR) instruments. MR images are based primarily on proton density and proton relaxation dynamics. MR instruments are sensitive to two different relaxation processes, the T1 (spin-lattice or longitudinal relaxation time) and T2 (spin-spin or transverse relaxation time). Paramagnetic agents contain one or more unpaired electrons that enhance the T1 and T2 relaxation rates of protons in their molecular environment. The proton relaxation effect (PRE) of an unpaired electron is 700 times stronger than that of a proton itself. In MRI, visualization of normal and pathological brain tissue depends in part on variations in the radio frequency signal intensity that occur with changes in proton density, alteration of the T1, and variation in T2. When placed in a magnetic field, gadopentetate dimeglumine shortens the T1 and T2 relaxation times in tissues where it accumulates. In the central nervous system (CNS), gadopentetate dimeglumine enhances visualization of normal tissues that lack a blood-brain barrier, such as the pituitary gland and the meninges. Gadopentetate dimeglumine does not cross the intact blood-brain barrier; therefore, it does not accumulate in normal brain tissue or in CNS lesions that have not caused an abnormal blood-brain barrier (e.g., cysts, mature post-operative scars). Abnormal vascularity or disruption of the blood-brain barrier allows accumulation of gadopentetate dimeglumine in lesions such as neoplasms, abscesses, and subacute infarcts. Outside the CNS, gadopentetate dimeglumine rapidly reaches equilibrium in the interstitial compartment and enhances signal in all tissues as a function of delivery and size of the interstitial compartment. Drug type: Approved. Small Molecule. Drug category: Contrast Agents. Contrast Media | ILX:0104522 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Gadoteridol | Gadoteridol provides contrast enhancement of the brain, spine and surrounding tissues resulting in improved visualization (compared with unenhanced MRI) of lesions with abnormal vascularity or those thought to cause a disruption of the normal blood brain barrier. Gadoteridol can also be used for whole body contrast enhanced MRI including the head, neck, liver, breast, musculoskeletal system and soft tissue pathologies. n MRI, visualization of normal and pathological brain tissue depends in part on variations in the radiofrequency signal intensity that occur with changes in proton density, alteration of the T1, and variation in T2. When placed in a magnetic field, gadoteridol shortens the T1 relaxation time in tissues where it accumulates. Abnormal vascularity or disruption of the blood-brain barrier allows accumulation of gadoteridol in lesions such as neoplasms, abscesses, and subacute infarcts. Pharmacology: Not Available Mechanism of action: Based on the behavior of protons when placed in a strong magnetic field, which is interpreted and transformed into images by magnetic resonance (MR) instruments. Paramagnetic agents have unpaired electrons that generate a magnetic field about 700 times larger than the proton's field, thus disturbing the proton's local magnetic field. When the local magnetic field around a proton is disturbed its relaxation process is altered. MR images are based on proton density and proton relaxation dynamics. MR instruments can record two different relaxation processes, the T1 (spin-lattice or longitudinal relaxation time) and T2 (spin-spin or transverse relaxation time). In MRI, visualization of normal and pathological brain tissue depends in part on variations in the radiofrequency signal intensity that occur with changes in proton density, alteration of the T1, and variation in T2. When placed in a magnetic field, gadoteridol shortens the T1 relaxation time in tissues where it accumulates. Gadoteridol does not cross the intact blood-brain barrier; therefore, it does not accumulate in normal brain tissue or in central nervous system (CNS) lesions that have not caused an abnormal blood-brain barrier (e.g., cysts, mature post-operative scars). Abnormal vascularity or disruption of the blood-brain barrier allows accumulation of gadoteridol in lesions such as neoplasms, abscesses, and subacute infarcts. Drug type: Approved. Small Molecule. Drug category: Contrast Agents. Contrast Media | ILX:0104523 | 4 | FDI Lab - SciCrunch.org | 08/24/2018 | FDI Lab - SciCrunch.org | term | 12/08/2016 | 0 | NeuroLex | troy sincomb |
| Gadoversetamide | Gadoversetamide is a gadolinium compound used as a contrast agent in magnetic resonance imaging (MRI), particularly imaging of the brain, spine and liver. It is marketed under the trade name OptiMARK. Pharmacology: Not Available Mechanism of action: Based on the behavior of protons when placed in a strong magnetic field, which is interpreted and transformed into images by magnetic resonance (MR) instruments. MR images are based primarily on proton density and proton relaxation dynamics. MR instruments are sensitive to two different relaxation processes, the T1 (spin-lattice or longitudinal relaxation time) and T2 (spin-spin or transverse relaxation time). Paramagnetic agents contain one or more unpaired electrons that enhance the T1 and T2 relaxation rates of protons in their molecular environment. In MRI, visualization of normal and pathological brain, spinal and hepatic tissue depends in part on variations in the radio frequency signal intensity that occur with changes in proton density, alteration of the T1, and variation in T2. When placed in a magnetic field, gadoversetamide shortens the T1 and T2 relaxation times in tissues where it accumulates. At the recommended dose, the effect is primarily on T1 relaxation time, and produces an increase in signal intensity (brightness). Gadoversetamide does not cross the intact blood-brain barrier; therefore, it does not accumulate in normal brain tissue or in CNS lesions that may have a normal blood-brain barrier (e.g., cysts, mature post-operative scars). Abnormal vascularity or disruption of the blood-brain barrier allows accumulation of gadoversetamide in lesions such as neoplasms, abscesses, and subacute infarcts. Drug type: Approved. Investigational. Small Molecule. Drug category: Contrast Agents. Contrast Media | ILX:0104524 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Gait Ataxia | Impairment of the ability to coordinate the movements required for normal ambulation ( WALKING) which may result from impairments of motor function or sensory feedback. This condition may be associated with BRAIN DISEASES (including CEREBELLAR DISEASES and BASAL GANGLIA DISEASES); SPINAL CORD DISEASES; or PERIPHERAL NERVOUS SYSTEM DISEASES (MeSH). | ILX:0104525 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| GAL1 receptor | ILX:0104526 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/08/2016 | 0 | NeuroLex | NeuroLex | |
| GAL2 receptor | ILX:0104527 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/08/2016 | 0 | NeuroLex | NeuroLex | |
| GAL3 receptor | ILX:0104528 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/08/2016 | 0 | NeuroLex | NeuroLex | |
| Galanin | [Adopted from Wikipedia]Galanin is a neuropeptide encoded by the GAL gene,[1] that is widely expressed in the brain, spinal cord, and gut of humans as well as other mammals. Galanin signaling occurs through three G protein-coupled receptors.[2]The functional role of galanin remains largely unknown; however, galanin is predominately involved in the modulation and inhibition of action potentials in neurons. Galanin has been implicated in many biologically diverse functions, including: nociception, waking and sleep regulation, cognition, feeding, regulation of mood, regulation of blood pressure, it also has roles in development as well as acting as a trophic factor.[3] Galanin is linked to a number of diseases including Alzheimer's disease, epilepsy as well as depression, eating disorders and cancer.[4][5] Galanin appears to have neuroprotective activity as its biosynthesis is increased 2-10 fold upon axotomy in the peripheral nervous system as well as when seizure activity occurs in the brain. It may also promote neurogenesis.[2]Galanin is predominantly an inhibitory, hyperpolarizing neuropeptide[6]and as such inhibits neurotransmitter release. Galanin is often co-localized with classical neurotransmitters such as acetylcholine, serotonin, and norepinephrine, and also with other neuromodulators such as Neuropeptide Y, Substance P, and Vasoactive intestinal peptide.[7][1] Evans H, Baumgartner M, Shine J, Herzog H (December 1993). "Genomic organization and localization of the gene encoding human preprogalanin". Genomics 18 (3): 473–7. PMID 7508413.[2] Mitsukawa K, Lu X, Bartfai T (June 2008). "Galanin, galanin receptors and drug targets". Cell. Mol. Life Sci. 65 (12): 1796–805. doi:10.1007/s00018-008-8153-8. PMID 18500647.[3] Mechenthaler I (June 2008). "Galanin and the neuroendocrine axes". Cell. Mol. Life Sci. 65 (12): 1826–35. doi:10.1007/s00018-008-8157-4. PMID 18500643.[4] Lundström L, Elmquist A, Bartfai T, Langel U (2005). "Galanin and its receptors in neurological disorders". Neuromolecular Med. 7 (1-2): 157–80. doi:10.1385/NMM:7:1-2:157. PMID 16052044.[5] Berger A, Santic R, Hauser-Kronberger C, Schilling FH, Kogner P, Ratschek M, Gamper A, Jones N, Sperl W, Kofler B (June 2005). "Galanin and galanin receptors in human cancers". Neuropeptides 39 (3): 353–9. doi:10.1016/j.npep.2004.12.016. PMID 15944034.[6] Ito M (September 2009). "Functional roles of neuropeptides in cerebellar circuits". Neuroscience 162 (3): 666–72. doi:10.1016/j.neuroscience.2009.01.019. PMID 19361475.[7] Bartfai, T., (2000). "Galanin – A neuropeptide with important central nervous system actions". Retrieved November 19, 2009. | ILX:0104529 | 5 | FDI Lab - SciCrunch.org | 01/17/2023 | FDI Lab - SciCrunch.org | term | 12/08/2016 | 0 | NeuroLex | troy sincomb |
| Galanin receptor | ILX:0104530 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/08/2016 | 0 | NeuroLex | NeuroLex | |
| Galantamine | A benzazepine derived from norbelladine. It is found in galanthus and other amaryllidaceae. It is a cholinesterase inhibitor that has been used to reverse the muscular effects of gallamine triethiodide and tubocurarine and has been studied as a treatment for alzheimer disease and other central nervous system disorders. (PubChem) Pharmacology: Galantamine is a parasympathomimetic, specifically, a reversible cholinesterase inhibitor. Galantamine is indicated for the treatment of mild to moderate dementia of the Alzheimer's type. Galantamine is postulated to exert its therapeutic effect by enhancing cholinergic function. This is accomplished by increasing the concentration of acetylcholine through reversible inhibition of its hydrolysis by acetylcholinesterase. If this proposed mechanism of action is correct, Galantamine's effect may lessen as the disease process advances and fewer cholinergic neurons remain functionally intact. There is no evidence that Galantamine alters the course of the underlying dementing process. Mechanism of action: Galantamine's proposed mechanism of action involves the increase of the concentration of acetylcholine through reversible inhibition of its hydrolysis by acetylcholinesterase. Drug type: Approved. Small Molecule. Drug category: Cholinesterase Inhibitors. Nootropic Agents. Parasympathomimetics | ILX:0104531 | 4 | FDI Lab - SciCrunch.org | 08/24/2018 | FDI Lab - SciCrunch.org | term | 12/08/2016 | 0 | NeuroLex | troy sincomb |
| Gallamine Triethiodide | A synthetic nondepolarizing blocking drug. The actions of gallamine triethiodide are similar to those of tubocurarine, but this agent blocks the cardiac vagus and may cause sinus tachycardia and, occasionally, hypertension and increased cardiac output. It should be used cautiously in patients at risk from increased heart rate but may be preferred for patients with bradycardia. (From AMA Drug Evaluations Annual, 1992, p198) Pharmacology: Gallamine Triethiodide is a nondepolarizing neuromuscular blocking drug (NDMRD) used as an adjunct to anesthesia to induce skeletal muscle relaxation. The actions of gallamine triethiodide are similar to those of tubocurarine, but this agent blocks the cardiac vagus and may cause sinus tachycardia and, occasionally, hypertension and increased cardiac output. Muscle groups differ in their sensitivity to these types of relaxants with ocular muscles (controlling eyelids) being most sensitive, followed by the muscles of the neck, jaw, limbs and then abdomen. The diaphragm is the least sensitive muscle to NDMRDs. Although the nondepolarizing neuromuscular blocking drugs do not have the same adverse effects as succinylcholine, their onset of action is slower. They also have a longer duration of action, making them more suitable for maintaining neuromuscular relaxation during major surgical procedures. Mechanism of action: It competes with acetylcholine (ACh) molecules and binds to muscarinic acetylcholine receptors on the post-synaptic membrane of the motor endplate. It blocks the action of ACh and prevents activation of the muscle contraction process. It can also act on nicotinic presynaptic acetylcholine receptors which inhibits the release of ACh. Drug type: Approved. Small Molecule. Drug category: Neuromuscular Nondepolarizing Agents. Nicotinic Antagonists. Skeletal Muscle Relaxants | ILX:0104532 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Galliformes | ILX:0104533 | 5 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/08/2016 | 0 | NeuroLex | NeuroLex | |
| Gallus | ILX:0104534 | 5 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/08/2016 | 0 | NeuroLex | NeuroLex | |
| Gallyas silver stain | Silver staining method for revealing neurofibrillary changes in the brains of patients with Alzheimer's disease and related models, developed by F. Gallyas. | ILX:0104535 | 4 | FDI Lab - SciCrunch.org | 08/24/2018 | FDI Lab - SciCrunch.org | term | 12/08/2016 | 0 | NeuroLex | troy sincomb |
| Galsulfase | Galsufase is a variant form of the polymorphic human enzyme N-acetylgalactosamine 4-sulfatase of recombinant DNA origin. Galsulfase is a glycoprotein with a molecular weight of approximately 56 kD. The recombinant protein is comprised of 495 amino acids and contains six asparagine-linked glycosylation sites, four of which carry a bis mannose-6-phosphate manose7 oligosaccharide for specific cellular recognition. Post-translational modification of Cys53 produces the catalytic amino acid residue Ca-formylglycine, which is required for enzyme activity and is conserved in all members of the sulfatase enzyme family. Pharmacology: Mucopolysaccharide storage disorders are caused by the deficiency of specific lysosomal enzymes required for the catabolism of GAG. Mucopolysaccharidosis VI (MPS VI, Maroteaux-Lamy syndrome) is characterized by the absence or marked reduction in N-acetylgalactosamine 4-sulfatase. The sulfatase activity deficiency results in the accumulation of the GAG substrate dermatan sulfate, throughout the body. This accumulation leads to widespread cellular, tissue, and organ dysfunction. Galsulfase is intended to provide an exogenous enzyme that will be taken up into lysosomes and increase the catabolism of GAG. Galsulfase uptake by cells into lysosomes is most likely mediated by the binding of mannose-6-phosphate-terminated oligosaccharide chains of galsulfase to specific mannose-6-phosphate receptors. Mechanism of action: Galsulfase supplies recombinant-engineered galsulfase, a normal variant form of the polymorphic human enzyme, N-acetylgalactosamine 4-sulfatase. It is a lysosomal hydrolase that catalyzes the cleavage of the sulfate ester from terminal N-acetylgalactosamine 4-sulfate residues of GAG chondroitin 4-sulfate and dermatan sulfate. Increased catabolism of GAG in turn reduces systemic dermatan sulfate accumulation, thereby reducing the primary symptoms of MPS VI. Drug type: Approved. Biotech. Investigational. Drug category: Enzyme Replacement Agents | ILX:0104536 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Gamma Hydroxybutyric Acid | Gamma Hydroxybutyric Acid, commonly abbreviated GHB, is a therapeutic drug which is illegal in multiple countries. It is currently regulated in the US and sold by Jazz Pharmaceuticals under the name Xyrem. However, it is important to note that GHB is a designated Orphan drug (in 1985). Today Xyrem is a Schedule III drug;however GHB remains a Schedule I drug and the illicit use of Xyrem falls under penalties of Schedule I. GHB is a naturally occurring substance found in the central nervous system, wine, beef, small citrus fruits and almost all other living creatures in small amounts. It is used illegally under the street names Juice, Liquid Ecstasy or simply G, either as an intoxicant, or as a date rape drug. Xyrem is a central nervous system depressant that reduces excessive daytime sleepiness and cataplexy in patients with narcolepsy. Pharmacology: Not Available Mechanism of action: Not Available Drug type: Approved. Illicit. Small Molecule. Drug category: Adjuvants, Anesthesia. Anesthetics, Intravenous | ILX:0104537 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
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