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Amantadine

Amantadine is a medication used to treat and prevent influenza A infections.
It works by interfering with the viral replication process, making it more difficult for the virus to infect host cells.
Amantadine may also be used off-label to manage symptoms of Parkinson's disease and other neurological disorders.
Researchers rely on PubCompare.ai to streamlien their Amantadine studies, locating the most effective protocols and produts to accelerate their work and enhance reproducibility.
The AI-driven platform leverages advanced analytics to optimize Amantadine research, ensuring improved efficiency and confidence in these important studies.

Most cited protocols related to «Amantadine»

1
Early Parkinson's Disease Cohort Study
Cited 48 times
PD and HC subjects of similar age and gender from 24 study sites in the US (18), Europe (5) and Australia (1) were enrolled after obtaining informed consent. We acknowledge that the early PD cohort likely includes a small number of subjects with other DAT deficit parkinsonian syndromes such as progressive supranuclear palsy (PSP), multiple system atrophy (MSA) and cortical basal syndrome (CBS), which may be indistinguishable from PD at the earliest stages of disease. At each study visit, the investigators reassess the subject diagnosis to identify any non‐PD subjects.
This study was conducted in accordance with the Declaration of Helsinki and the Good Clinical Practice (GCP) guidelines after approval of the local ethics committees of the participating sites. At enrollment, PD subjects were required to be age 30 years or older, untreated with PD medications (levodopa, dopamine agonists, MAO‐B inhibitors, or amantadine), within 2 years of diagnosis, Hoehn and Yahr <3, and to have either at least two of resting tremor, bradykinesia, or rigidity (must have either resting tremor or bradykinesia) or a single asymmetric resting tremor or asymmetric bradykinesia. All PD subjects underwent dopamine transporter (DAT) imaging with 123I Ioflupane or vesicular monoamine transporter (VMAT‐2) imaging with 18F AV133 (Australia only) and were only eligible if DAT or VMAT‐2 imaging demonstrated dopaminergic deficit consistent with PD in addition to clinical features of the disease. Study investigators evaluated enrolled PD subjects to assess absence of current or imminent (6 months) disability requiring PD medications, though subjects could initiate PD medications at any time after enrollment if the subject or investigator deemed it clinically necessary. Those subjects screened as potential PD subjects who were ineligible due to DAT or VMAT‐2 scans without evidence of dopaminergic deficit (SWEDD) were eligible to be enrolled in a SWEDD cohort.4 HC subjects were required to be age 30 years or older without an active, clinically significant neurological disorder or a first‐degree relative with PD. All enrolled subjects agreed to complete all study evaluations, including lumbar puncture.
PD and SWEDD subjects were excluded if they had a clinical diagnosis of dementia or had taken PD medications within 60 days of baseline or for longer than 60 days in total. HC subjects were excluded if they had a Montreal Cognitive Assessment (MoCA) total score ≤26. All subjects were excluded if they were treated with neuroleptics, metoclopramide, alpha methyldopa, methylphenidate, reserpine, or amphetamine derivative within 6 months or were currently treated with anticoagulants that might preclude safe completion of the lumbar puncture.
Marek K., Chowdhury S., Siderowf A., Lasch S., Coffey C.S., Caspell‐Garcia C., Simuni T., Jennings D., Tanner C.M., Trojanowski J.Q., Shaw L.M., Seibyl J., Schuff N., Singleton A., Kieburtz K., Toga A.W., Mollenhauer B., Galasko D., Chahine L.M., Weintraub D., Foroud T., Tosun‐Turgut D., Poston K., Arnedo V., Frasier M, & Sherer T. (2018). The Parkinson's progression markers initiative (PPMI) – establishing a PD biomarker cohort. Annals of Clinical and Translational Neurology, 5(12), 1460-1477.
Publication 2018
123I-ioflupane Amantadine Amphetamine Anticoagulants Antipsychotic Agents Bradykinesia Cortex, Cerebral Dementia Diagnosis Disabled Persons Dopamine Agonists Gender Hydrochloride, Dopamine Levodopa Methyldopa Methylphenidate Metoclopramide Monoamine Oxidase Inhibitors Multiple System Atrophy Muscle Rigidity Nervous System Disorder Parkinsonian Disorders Pharmaceutical Preparations Progressive Supranuclear Palsy Punctures, Lumbar Radionuclide Imaging Regional Ethics Committees Reserpine Resting Tremor SLC6A3 protein, human Syndrome Vesicular Monoamine Transport Proteins Volumetric-Modulated Arc Therapy
2
Xenopus Oocyte Electrophysiology with Amantadine
Cited 13 times
Stage V–VI Xenopus laevis oocytes were prepared as described previously (30 (link)). Oocytes injection and TEVC electrophysiological measurements were done as previously described (29 (link)). Amantadine (Sigma, St. Louis, MO) was applied to inhibit A/M2 induced currents. Data were analyzed using ORIGIN 8.0 software (OriginLab, Northampton, MA).
Balannik V., Wang J., Ohigashi Y., Jing X., Magavern E., Lamb R.A., DeGrado W.F, & Pinto L.H. (2009). Design and Pharmacological Characterization of Inhibitors of Amantadine-Resistant Mutants of the M2 Ion Channel of Influenza A Virus. Biochemistry, 48(50), 11872-11882.
Publication 2009
Amantadine Cardiac Arrest Oocytes Xenopus laevis
3
Tracking Influenza Sentiment via Twitter
Cited 10 times
In order to explore public concerns regarding rapidly evolving H1N1 activity, we
collected and stored a large sample of public tweets beginning April 29, 2009
that matched a set of pre-specified search terms: flu, swine, influenza,
vaccine, tamiflu, oseltamivir, zanamivir, relenza, amantadine, rimantadine,
pneumonia, h1n1, symptom, syndrome, and illness.
Additional keywords were used to examine other aspects of public concern,
including disease transmission in particular social contexts (i.e., keywords
travel, trip, flight, fly, cruise and
ship), disease countermeasures (i.e., keywords wash,
hand, hygiene and mask), and consumer concerns
about pork consumption (i.e., keywords pork and
bacon). Each tweet is time-stamped and geolocated using the
author's self-declared home location. A client-side JavaScript application
was created to display a continuously-updated Google map with the 500 most
recently matched tweets, yielding a real-time view of flu-related public
sentiment in geographic context. Anyone visiting the web site could read any
tweet by placing the cursor over its corresponding color-coded (by search terms)
dot on the map (Figure
1).
Beginning on October 1, 2009, we collected an expanded sample of tweets using
Twitter's new streaming application programmer's interface (API) [10] with the
intent of estimating influenza activity. In addition, following discussions with
public health officials, new search terms were added to investigate concerns
about vaccine side effects and/or vaccine shortages: guillain,
barré, barre, shortage, hospital, and
infection.
Note that the Twitter stream is filtered in accordance with Twitter's API
documentation; hence the tweets analyzed here still constitute a representative
subset of the stream as opposed to the entire stream.
Moreover, because our main interest was to monitor influenza-related traffic
within the United States, we also excluded all tweets tagged as originating
outside the U.S., tweets from users with a non-U.S. timezone, and any tweets not
written in English. We also excluded all tweets having less than 5 characters,
those containing non-ASCII characters, and tweets sent by a client identifying
itself as “API” (the latter are usually generated by computer and
therefore tend to be “spam”). The remaining tweets were used to
produce a dictionary of English words, from which all commonly-used keywords
comprising Twitter's informal messaging conventions (e.g., #hashtag, @user,
RT, links, etc.) were removed. Porter's Stemming Algorithm [11] was
used to reduce inflected words to their root forms (e.g., “knowing”
becomes “know”) in order to compress the size of the dictionary. We
then compiled daily and weekly usage statistics for each dictionary term (i.e.,
number of tweets in which each term occurred), both nationally (by aggregating
data for all valid locations) and at the CDC's influenza reporting region
level [12] .
Finally, because the volume of posts on Twitter varies over time as well as
across geographic regions, usage statistics were expressed in terms of the
fraction of the total tweets emitted within the corresponding time interval and
geographic region.
Signorini A., Segre A.M, & Polgreen P.M. (2011). The Use of Twitter to Track Levels of Disease Activity and Public Concern in the U.S. during the Influenza A H1N1 Pandemic. PLoS ONE, 6(5), e19467.
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Publication 2011
Amantadine Character Conferences Guillain-Barre Syndrome Oseltamivir Pigs Plant Roots Pneumonia Pork Relenza Rimantadine Stem, Plant Syndrome Tamiflu Temporal Lobe Transmission, Communicable Disease Vaccines Virus Vaccine, Influenza Zanamivir
4
Solid-State NMR of Influenza M2 Protein
Cited 10 times
The TM domain of the M2 protein of the Udorn strain (residues 22–46, SSDPLVVAASII GILHLILWILDRL) was synthesized by Fmoc chemistry and purified to >95% purity. Two peptide samples containing eight uniformly 13C, 15N-labeled residues were used. The labeled sites are L26, A29, G34 and I35 in one sample (LAGI), and V27, A30, I33 and L38 in the other (VAIL).
Egg sphingomyelin (SM) was dissolved in chloroform/methanol (10:2) solution, and mixed with DPPC, DPPE and Chol at a molar ratio of SM: DPPC: DPPE : Chol = 28% : 21% : 21% : 30%. The membrane mixture was lyophilized, dissolved in pH 7.5 phosphate buffer, vortexed, and freeze-thawed several times to form large unilamellar vesicles. The membrane has a broad phase transition around 243 K based on static 31P spectra (Supporting Information Fig. S1).
AM2-TM was reconstituted into the viral membrane mixture by detergent dialysis as described before (23 (link)). The peptide : lipid molar ratios was 1:15 – 1:12. The proteoliposomes were centrifuged at 150,000 g to obtain the membrane pellet. Photometric assay showed >95% binding of the peptide. The pellet was packed into 4 mm MAS rotors for NMR experiments. For the amantadine-bound sample, amantadine hydrochloride in the pH 7.5 buffer was directly titrated to the pellet at a peptide: amantadine molar ratio of 1: 2.
Luo W., Cady S.D, & Hong M. (2009). Immobilization of the Influenza A M2 Transmembrane Peptide in Virus-Envelope Mimetic Lipid Membranes: A Solid-State NMR Investigation. Biochemistry, 48(27), 6361-6368.
Publication 2009
Amantadine Biological Assay bis(diphenylphosphine)ethane Buffers Chloroform Detergents Dialysis Freezing Hydrochloride, Amantadine Lipids Methanol Molar Peptides Phase Transition Phosphates Photometry Protein Domain proteoliposomes Sphingomyelins Strains Tissue, Membrane Unilamellar Vesicles
5
Evaluating M2 and M1 Antibody Responses
Cited 9 times
Blood samples were collected before and at 3 weeks after each immunization and stored −20°C until analysis. M2 specific serum antibody responses were determined by ELISA using synthetic M2e peptide or inactivated purified virions (2 µg/ml) as a coating antigen as previously described [26] (link), [49] (link). Briefly, HRP-conjugated goat anti-mouse IgG, IgG1 and IgG2a were used as secondary antibodies to determine total IgG and isotype antibodies. The substrate O-phenylenediamine (OPD) (Zymed, San Francisco, Calif.) in citrate-phosphate buffer (pH 5.0) containing 0.03% H2O2 (Sigma) was used to develop color. The optical density at 450 nm was read using an ELISA reader.
M2 expressing MDCK cells [50] (link) were maintained in DMEM media with 7.5 µg/ml of puromycin (Invitrogen, Carlsbad, CA), 5 µM of amantadine (Sigma, St. Louis, MO) and 10% FBS (Invitrogen, Carlsbad, CA) at 37°C in air/CO2. Confluent M2 expressing MDCK monolayer cells were fixed by 0.05% glutaraldehyde or 10% buffered formalin (Sigma, St. Louis, MO) for 30 min at room temperature and used to determine antibody levels binding to M2 expressed on cell surfaces by ELISA as described [22] (link). M1 specific antibody responses were determined using the M1 protein peptide pool (2 µg/ml) derived from influenza A/New York/348/2003 (H1N1) virus (BEI resources, Manassas, VA).
Song J.M., Wang B.Z., Park K.M., Van Rooijen N., Quan F.S., Kim M.C., Jin H.T., Pekosz A., Compans R.W, & Kang S.M. (2011). Influenza Virus-Like Particles Containing M2 Induce Broadly Cross Protective Immunity. PLoS ONE, 6(1), e14538.
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Publication 2011
1,2-diaminobenzene Amantadine anti-IgG Antibodies Antibody Formation Antigens BLOOD Cells Citrates Enzyme-Linked Immunosorbent Assay Formalin Glutaral Goat IgG1 IgG2A Immunization Immunoglobulin Isotypes Immunoglobulins Influenza A Virus, H1N1 Subtype Madin Darby Canine Kidney Cells Mus Peptides Peroxide, Hydrogen Phosphates Proteins Puromycin Serum Virion Virus Vaccine, Influenza Vision

Most recents protocols related to «Amantadine»

1
Assessing Parkinson's Disease Profiles
The included patients were on stable medication before undergoing LCT (68 patients received L-dopa, 28 received amantadine, 29 received dopamine agonists, 9 were treated with monoamine oxidase B [MAO-B] inhibitors, and 5 used a catechol-o-methyltransferase inhibitor). Their demographic data, history of hypertension, use of antihypertensive drugs, age of onset, Hoehn and Yahr stage, disease duration, and use of anti-PD drugs were recorded. The L-dopa equivalent daily dose was calculated using a formula described previously.[14 (link)] Clinical features were assessed using the Movement Disorder Society Unified Parkinson’s Disease Rating Scale. Motor phenotypes were divided into postural instability and gait difficulty-dominant and non-postural instability and gait difficulty-dominant based on the Movement Disorder Society Unified Parkinson’s Disease Rating Scale scores.[15 (link)] Validated scales, including cognitive functions by the Montreal Cognitive Assessment (MoCA)-Beijing version,[16 (link)] anxiety by the Hamilton Anxiety Scale,[17 (link)] depression by the Hamilton Depression Scale,[18 (link)] quality of life by the 39-item Parkinson’s Disease Questionnaire,[19 (link)] autonomic functions by the Non-Motor Symptoms Questionnaire,[20 (link)] and sleep problems by the Parkinson’s Disease Sleep Scale,[21 (link)] were applied to evaluate patients’ non-motor symptoms.
Su D., Su Y., Xu B., Chhetri J.K, & Chan P. (2023). Age as a risk factor for orthostatic hypotension induced by the levodopa challenge test in patients with Parkinson’s disease: Results from a single-center trial. Medicine, 102(9), e33161.
Publication 2023
Amantadine Antihypertensive Agents Anxiety Cognition Dopamine Agonists Dyssomnias High Blood Pressures Levodopa Melancholia Monoamine Oxidase Inhibitors Movement Movement Disorders Nervous System, Autonomic O-Methyltransferase Inhibitors, Catechol Parkinson Disease Patients Pharmaceutical Preparations Phenotype
2
Disease-Modifying Potential of Isradipine and Inosine in Early Parkinson's Disease
Both trials were conducted at PSG sites. The PSG is an independent consortium of scientific investigators committed to the cooperative planning, implementation, analysis, and reporting of controlled clinical trials and other research in PD and related disorders.
STEADY-PD III was a phase 3, randomized, 2-arm, parallel-group, placebo-controlled, double-blind, multicenter clinical trial designed to assess the disease-modifying potential of isradipine in patients with early PD not receiving or requiring symptomatic therapy at baseline other than a stable dose of amantadine or anticholinergics. Participants were randomized 1:1 to receive either isradipine 5 mg twice daily or placebo for 36 months. Northwestern University served as the Clinical Coordination Center (CCC); the University of Rochester Clinical Trials Coordination Center served as the Data Coordination Center (DCC).8 (link) Inclusion criteria included age greater than 30 years, a PD diagnosis made within 3 years of screening, and not receiving excluded symptomatic PD therapy.9 (link) Exclusion criteria included history of significant cardiovascular disease, unstable medical or psychiatric conditions, significant cognitive impairment, use of calcium channel blockers, or other use of antihypertensives that would make exposure to isradipine unsafe.
SURE-PD3 was a phase 3, randomized, 2-arm, parallel-group, placebo-controlled, double-blind, 2-period, multicenter clinical trial designed to assess the disease-modifying potential of inosine in patients with early PD not receiving or requiring symptomatic therapy at baseline other than a stable dose of a monoamine oxidase–B inhibitor. Participants were randomized 1:1 to receive either oral inosine titrated to achieve a serum urate level from 7.1 to 8.0 mg/dL or placebo for 24 months. Massachusetts General Hospital served as the CCC; the University of Rochester served as the DCC.10 (link) Inclusion criteria included age greater than 30 years, a PD diagnosis made within 3 years of the screening visit, not receiving excluded symptomatic PD therapy, and serum urate ≤5.7 mg/dL. Exclusion criteria included history of significant cardiovascular disease, unstable medical or psychiatric conditions, significant cognitive impairment, use of thiazide diuretics, and history of crystallopathy or increased risk of crystallopathy due to low urine pH or renal impairment.
Di Luca D.G., Macklin E.A., Hodgeman K., Lopez G., Pothier L., Callahan K.F., Lowell J., Chan J., Videnovic A., Lungu C., Lang A.E., Litvan I., Schwarzschild M.A, & Simuni T. (2023). Enrollment of Participants From Marginalized Racial and Ethnic Groups: A Comparative Assessment of the STEADY-PD III and SURE-PD3 Trials. Neurology: Clinical Practice, 13(1), e200113.
Publication 2023
Amantadine Anticholinergic Agents Antihypertensive Agents Calcium Channel Blockers Cardiovascular Diseases Diagnosis Disorders, Cognitive Inosine Isradipine Mental Disorders Monoamine Oxidase B Patients Placebos Renal Insufficiency Serum Therapeutics Thiazide Diuretics Urate Urine
3
Cellular Uptake of Azacitidine Kinetics
IUR [40 (link)] were performed in triplicate with 2 × 105 cells per tube. Briefly, 2 × 105 cells were incubated for 2 h at 37 °C in the presence and absence of a 50% 14C-labeled 2 μM AZA. For IUR with inhibitors, 100 μM verapamil (Royal Adelaide Hospital Pharmacy, Adelaide, SA, Australia), 200 μM procainamide (Sigma-Aldrich, St. Louis, MO, USA), 10 μM corticosterone (Sigma-Aldrich, St. Louis, MO, USA), 20 μM NBMPR (Sigma-Aldrich, St. Louis, MO, USA), 20 μM cyclosporin A (Sigma-Aldrich, St. Louis, MO, USA), 10 μM chloroquine (Sigma-Aldrich, St. Louis, MO, USA), 150 μM amantadine (Sigma-Aldrich, St. Louis, MO, USA), 20 and 200 μM cimetidine (Sigma-Aldrich, St. Louis, MO, USA), and 0.1 and 10 μM pyrimethamine (Sigma-Aldrich, St. Louis, MO, USA) were added. After incubation the cellular and aqueous phases were separated, and incorporation determined using a Perkin Elmer Liquid Scintillation Analyser following the addition of Microscint 20 scintillation fluid (Perkin Elmer, Waltham, MA, USA) before counts per minute of β radiation in the supernatant and cell pellet fractions was used to convert to ng of AZA in 2 × 105 cells. All assays were performed in triplicate and repeated if the assay demonstrated non-concordance.
Kutyna M.M., Loone S., Saunders V.A., White D.L., Kok C.H, & Hiwase D.K. (2023). Solute Carrier Family 29A1 Mediates In Vitro Resistance to Azacitidine in Acute Myeloid Leukemia Cell Lines. International Journal of Molecular Sciences, 24(4), 3553.
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Publication 2023
4-nitrobenzylthioinosine Amantadine Beta Particle Biological Assay Cells Chloroquine Cimetidine Corticosterone Cyclosporine inhibitors Procainamide Pyrimethamine Verapamil
4
Molecular Docking of SARS-CoV-2 E Protein
Molecular docking studies of the 2155 ligands were carried out using Autodock Vina (version 1.2) program [73 (link)]. The docking procedure was validated by comparing the molecular interactions of amantadine on SARS-CoV-2 reported previously [74 (link)]. For all the docking simulations, the E protein was rigid and the ligands flexible. The drugs with the highest affinity and those that reach key amino acids that influence the E protein function were selected. Docking analyses were carried out on homopentameric and monomeric forms of E protein. For the case of homopentameric E protein, dockings were focused to the ionic channel (active site is formed by the following residues: Glu8, Thr11, Leu12, Val14, Asn15, Val17, Leu18, Leu19, Phe20, Leu21, Ala22, Phe23, Val24, Val25, Phe26, Leu27, Leu28, Val29, Thr30, Leu31, Ala32, Ile33, Leu34, Thr35, Ala36, Leu37, Arg38, Leu39, Ala40, Tyr42, Ala43, Ala44, Ile46, Val47, Val49, Leu51, Pro54, Val56, Tyr57, Ser60, Arg61, Lys63, Asn64 and Leu65) as well as the N-terminal region (residues 7 to 12). For both conformations of the monomeric form, dockings were focused to the C-terminal segment (residues 70 to 75). The docking process on the homopentamer (ionic channel) was carried out considering the following parameters: grid box (25.0 Å × 30.0 Å × 30.0 Å) centered at (40.0, 63.0, 55.0) Å, and for the N-terminal: grid box (20.0 Å × 40.0 Å × 20.0 Å) centered at (20.0, 63.0, 55.0) Å. For the monomeric C-terminal harpin, grid box (25 Å × 25 Å × 25 Å) centered at (−20.0, 5.0, −1.0) Å, and finally for the C terminal region conformation (exposed to the solvent), a grid box (25 Å × 25 Å × 25 Å) centered at (−20.0, 5.0, −1.0) Å. For all the procedures, an implicit solvent function was employed, as well as the following parameters: num_modes = 100, energy_range = 6 and exhaustiveness = 25, and Monte Carlo force field. At the end of this procedure, the conformation that showed the highest Gibbs free energy was selected for further studies [75 (link)].
Ramírez Salinas G.L., López Rincón A., García Machorro J., Correa Basurto J, & Martínez Archundia M. (2023). In Silico Screening of Drugs That Target Different Forms of E Protein for Potential Treatment of COVID-19. Pharmaceuticals, 16(2), 296.
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Publication 2023
Amantadine Amino Acids Ion Channel Ligands Muscle Rigidity Pharmaceutical Preparations Proteins SARS-CoV-2 Solvents
5
SNCA Gene Methylation Analysis in Parkinson's and MSA
We recruited 82 patients with a diagnosis of PD, including 41 women and 41 men (age: 62 [54.5; 67] years). The diagnosis was determined according to the criteria of International Parkinson and Movement Disorder Society [44 (link)]. Age at the disease onset was 55 [48; 62] years, and the disease duration was 4 [3; 8] years. The distribution of PD patients by Hoehn–Yahr scale was as follows: stage 1—14 patients (17.2%); stage 2—26 (31.6%); stage 3—40 (48.8%); and stage 4—2 (2.4%). Mean score on UPDRS-III was 45 [22; 56]. The majority of patients (64 patients, 78%) received antiparkinsonian therapy: levodopa therapy—44 (53.7%) patients, dopamine receptor agonists—40 (48.8%) patients, and amantadine—31 (37.8%) patients.
The MSA group included 24 patients with a parkinsonian phenotype (MSA-P): 7 men and 17 women aged 58.5 [55.5; 69] years. The diagnosis was determined according to the criteria of International Parkinson and Movement Disorder Society [17 (link)]. In MSA group the age at the disease onset was 55 [52; 64] years, and the disease duration 3.5 [2; 5.25] years.
A control group included 50 neurologically healthy volunteers (31 women, 19 men; age: 58.5 [53; 62.75] years). All three groups were sex- and age-matched.
The location of studied CpG sites in a reference genome (GRCh38) is presented in Appendix A and Appendix B. Methylation level was determined in the promoter region (at the 5′-end, CpG 3–9, numbering of CpG sites from the beginning of the promoter region), at the 3′-end of intron 1 (CpG 21–48 of 48, numbering from the beginning of intron 1), and in intron 2 (CpG 1–2 of 2) of the SNCA gene. As preliminary experiments showed that the region of the 5′-end of intron 1 of SNCA (CpG 1–20) was demethylated both in patients and in controls, we did not further study the methylation level in these CpG sites.
In addition to CpG sites, we also searched for and analyzed non-CpG sites (CpH sites). Non-CpG sites were detected by sequence analysis of methylated cytosine (mC) preceding adenine, thymine, or cytosine (mCA, mCT, and mCC, respectively). In the promoter region of the SNCA gene, clustered non-CpG methylation sites (28 non-CpG sites) were found, which were also analyzed. (Non-CpG sites were marked by a combination of the number of the preceding CpG site and a Latin letter in alphabetical order.) A search was also conducted for non-CpG sites in intron 1 and intron 2 of the SNCA gene, but no such non-CpG sites were found in this region in a group of patients and healthy volunteers.
Genomic DNA samples were obtained from peripheral blood leukocytes by Wizard Genomic DNA Purification Kit (Promega, USA) and underwent bisulfite conversion using the EZ DNA Methylation Kit (Zymo Research, USA). Then, the converted gDNA was used as template for PCR amplification. Primers flanking the studied regions were selected using the MethPrimer software, and their synthesis was performed in Syntol company (Moscow). The primer design is shown in Table 3.
Analysis of the methylation of the SNCA gene was carried out by direct Sanger sequencing. Sequences were analyzed on ABI Prism 3130 analyzer (Applied Biosystems) using Data Collection Software v3.0. The level of methylation was defined by analyzing Sanger sequencing results. The percentage of methylation for each CpG site for each DNA sample was calculated as a ratio of a blue peak «C» height (this peak indicates the presence of a methylated cytosine) to a sum of «C+T» blue and red peaks height in this position (methylated blue and unmethylated red cytosine). For non-CpG sites, the calculation was carried out similarly. The assessment was performed using the SeqBase computer program developed at Research Centre of Medical Genetics (Moscow). This program takes into account the non-equivalence of sequenced nucleotide composition as a result of a bisulfite conversion [45 (link)].
Statistical analysis was performed in Statistica 13.3 (TIBCO Software Inc.). To compare two independent groups, the Mann–Whitney U-test was used. To compare several independent groups, the Kruskal–Wallis test was used. Correlation analysis was carried out using Spearman’s rank test. The correlation was assessed as weak, with r ranged from 0.3 to 0.5 (and was not taken into account in the study), moderate with r = 0.5–0.7, and strong with r = 0.7–0.9. Results were considered statistically significant if p < 0.05. A Bonferroni correction was applied due to multiple comparisons. Therefore, statistical significance level for promoter 28 CpG sites and 28 non-CpG sites was 0.007; for 7 CpG sites of intron 1 was 0.0017; and for 2 CpG sites of intron 2 was 0.025.
Fedotova E.Y., Iakovenko E.V., Abramycheva N.Y, & Illarioshkin S.N. (2023). SNCA Gene Methylation in Parkinson’s Disease and Multiple System Atrophy. Epigenomes, 7(1), 5.
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Publication 2023
21-chloropregnenolone Adenine alpha-Synuclein Amantadine Anabolism Antiparkinson Agents CPG-ODN Cytosine Debility Diagnosis DNA Methylation Dopamine Agonists Genes Genome Healthy Volunteers hydrogen sulfite Introns Leukocytes Levodopa Movement Disorders Oligonucleotide Primers Patients Phenotype prisma Promega Therapeutics Thymine Woman

Top products related to «Amantadine»

1
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2
Ribavirin by Merck Group
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Sourced in United States
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9
Fetal bovine serum (fbs) by Thermo Fisher Scientific
Sourced in United States, China, United Kingdom, Germany, Australia, Japan, Canada, Italy, France, Switzerland, New Zealand, Brazil, Belgium, India, Spain, Israel, Austria, Poland, Ireland, Sweden, Macao, Netherlands, Denmark, Cameroon, Singapore, Portugal, Argentina, Holy See (Vatican City State), Morocco, Uruguay, Mexico, Thailand, Sao Tome and Principe, Hungary, Panama, Hong Kong, Norway, United Arab Emirates, Czechia, Russian Federation, Chile, Moldova, Republic of, Gabon, Palestine, State of, Saudi Arabia, Senegal
Fetal Bovine Serum (FBS) is a cell culture supplement derived from the blood of bovine fetuses. FBS provides a source of proteins, growth factors, and other components that support the growth and maintenance of various cell types in in vitro cell culture applications.
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Acetic acid by Merck Group
Sourced in United States, Germany, United Kingdom, Italy, India, China, France, Spain, Switzerland, Poland, Sao Tome and Principe, Australia, Canada, Ireland, Czechia, Brazil, Sweden, Belgium, Japan, Hungary, Mexico, Malaysia, Macao, Portugal, Netherlands, Finland, Romania, Thailand, Argentina, Singapore, Egypt, Austria, New Zealand, Bangladesh
Acetic acid is a colorless, vinegar-like liquid chemical compound. It is a commonly used laboratory reagent with the molecular formula CH3COOH. Acetic acid serves as a solvent, a pH adjuster, and a reactant in various chemical processes.

More about "Amantadine"

Amantadine is a versatile medication with a wide range of applications.
As an antiviral agent, it is used to treat and prevent influenza A infections by interfering with the viral replication process, making it more difficult for the virus to infect host cells.
Additionally, amantadine may be utilized off-label to manage symptoms of Parkinson's disease and other neurological disorders.
Researchers often rely on advanced AI-driven platforms like PubCompare.ai to streamline their amantadine studies.
This innovative tool helps scientists locate the most effective protocols and products from literature, pre-prints, and patents, accelerating their research and enhancing reproducibility.
By leveraging advanced analytics, PubCompare.ai identifies the optimal amantadine protocols and products, ensuring improved efficiency and confidence in these important studies.
Amantadine is closely related to other compounds like ribavirin, formic acid, and 1-adamantylamine, which may share similar properties or be used in combination therapies.
Additionally, common laboratory techniques such as the use of 96-well plates, sodium hydroxide, and cell culture media like DMEM and FBS may be employed in amantadine research.
Acetic acid and memantine are also relevant terms that may be associated with amantadine studies.
By incorporating these synonyms, related terms, abbreviations, and key subtopics, researchers can optimize their search and discover the most relevant information to support their amantadine-focused work.
Leveraging the power of AI-driven platforms like PubCompare.ai can help accelerate the pace of amantadine research and enhance the overall confidence and reproducibility of these important studies.