quinacrine has been researched along with Dementias, Transmissible in 34 studies
Quinacrine: An acridine derivative formerly widely used as an antimalarial but superseded by chloroquine in recent years. It has also been used as an anthelmintic and in the treatment of giardiasis and malignant effusions. It is used in cell biological experiments as an inhibitor of phospholipase A2.
quinacrine : A member of the class of acridines that is acridine substituted by a chloro group at position 6, a methoxy group at position 2 and a [5-(diethylamino)pentan-2-yl]nitrilo group at position 9.
| Excerpt | Relevance | Reference |
|---|---|---|
| "We previously reported that quinacrine inhibited the formation of an abnormal prion protein (PrPres), a key molecule in the pathogenesis of transmissible spongiform encephalopathy, or prion disease, in scrapie-infected neuroblastoma cells." | 3.72 | Quinoline derivatives are therapeutic candidates for transmissible spongiform encephalopathies. ( Doh-Ura, K; Ishikawa, K; Iwaki, T; Kawatake, S; Kira, J; Murakami-Kubo, I; Ohta, S; Sasaki, K, 2004) |
| " The primary endpoints were death and serious adverse events possibly or probably related to the study drug." | 2.74 | Safety and efficacy of quinacrine in human prion disease (PRION-1 study): a patient-preference trial. ( Collinge, J; Darbyshire, J; Gorham, M; Hudson, F; Kennedy, A; Keogh, G; Pal, S; Rossor, M; Rudge, P; Siddique, D; Spyer, M; Thomas, D; Walker, S; Webb, T; Wroe, S, 2009) |
| "Quinacrine was reported to have a marked in vitro antiprion action in mouse neuroblastoma cells." | 2.71 | A possible pharmacological explanation for quinacrine failure to treat prion diseases: pharmacokinetic investigations in a ovine model of scrapie. ( Andréoletti, O; Gayrard, V; Laroute, V; Picard-Hagen, N; Toutain, PL; Viguié, C, 2005) |
| "Prion diseases are fatal infectious neurodegenerative disorders; examples include the Creutzfeldt-Jakob disease affecting humans and bovine spongiform encephalopathy in cattle." | 2.45 | [Systematic review of the therapeutics for prion diseases]. ( Sakaguchi, S, 2009) |
| "The pathogenesis of prion disease is the conversion of a normal type prion protein (PrP(C)) into a pathological isoform with protease resistance (PrP(Sc)), which accumulates in the brain." | 1.42 | [Current Trends in the Treatment of Prion Disease]. ( Tsuboi, Y, 2015) |
| "Since the infectious pathogen of prion diseases is composed of multimeric PrP(Sc) assemblies, we hypothesized that this antiprion property could be enhanced by attaching multiple quinacrine-derived chloroquinoline or acridine moieties to a scaffold." | 1.38 | Prion inhibition with multivalent PrPSc binding compounds. ( Genovesi, S; Joy, S; Li, L; Mays, CE; West, FG; Westaway, D; Yu, L, 2012) |
| "Human prion diseases are heterogeneous but invariably fatal neurodegenerative disorders with no known effective therapy." | 1.37 | PRION-1 scales analysis supports use of functional outcome measures in prion disease. ( Collinge, J; Darbyshire, JH; Gopalakrishnan, GS; Hudson, F; Kennedy, A; MacKay, A; Mead, S; Ranopa, M; Rudge, P; Thompson, AG; Walker, AS; Wroe, S, 2011) |
| "Treatment with quinacrine did not prolong the survival times of prion-inoculated, wild-type or MDR(0/0) mice compared to untreated mice." | 1.35 | Continuous quinacrine treatment results in the formation of drug-resistant prions. ( Ahn, M; DeArmond, SJ; Ghaemmaghami, S; Giles, K; Legname, G; Lessard, P; Prusiner, SB, 2009) |
| "Prion diseases are a group of fatal neurodegenerative diseases affecting humans and animals." | 1.35 | Chemically induced accumulation of GAGs delays PrP(Sc) clearance but prolongs prion disease incubation time. ( Avrahami, D; Friedman-Levi, Y; Gabizon, R; Mayer-Sonnenfeld, T, 2008) |
| "Prion diseases are characterized by an accumulation of PrP(Sc), a misfolded isoform of the normal cellular prion protein, PrP(C)." | 1.32 | Potent inhibition of scrapie prion replication in cultured cells by bis-acridines. ( Cohen, FE; Deady, LW; Fafarman, AT; Hong, SB; May, BC; Prusiner, SB; Rogers, M, 2003) |
| "3." | 1.32 | Uptake and efflux of quinacrine, a candidate for the treatment of prion diseases, at the blood-brain barrier. ( Dohgu, S; Higuchi, S; Katamine, S; Kataoka, Y; Naito, M; Niwa, M; Sawada, Y; Shirabe, S; Takata, F; Tsuruo, T; Yamauchi, A, 2004) |
| "Quinacrine was demonstrated to penetrate rapidly into brain tissue, achieving concentrations up to 1500 ng/g, which is several-fold greater than that demonstrated to inhibit formation of PrPSc in cell culture." | 1.32 | Pharmacokinetics of quinacrine in the treatment of prion disease. ( Baldwin, M; Guglielmo, BJ; Huang, Y; Legname, G; Lessard, P; Lin, ET; Prusiner, SB; Ryou, C; Yung, L, 2004) |
| " Previous studies have shown that N-methyl-D-aspartate (NMDA) receptor antagonists can inhibit glutathione depletion and neurotoxicity induced by PrP(TSE) and a toxic prion protein peptide, PrP106-126, in vitro." | 1.31 | Involvement of the 5-lipoxygenase pathway in the neurotoxicity of the prion peptide PrP106-126. ( Beyreuther, K; Cappai, R; Collins, SJ; Jobling, MF; Maher, F; Masters, CL; Needham, BE; Stewart, LR; Thyer, J; White, AR, 2001) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 23 (67.65) | 29.6817 |
| 2010's | 10 (29.41) | 24.3611 |
| 2020's | 1 (2.94) | 2.80 |
| Authors | Studies |
|---|---|
| Nguyen, TH | 1 |
| Lee, CY | 1 |
| Teruya, K | 1 |
| Ong, WY | 1 |
| Doh-ura, K | 6 |
| Go, ML | 2 |
| Thompson, MJ | 1 |
| Borsenberger, V | 1 |
| Louth, JC | 1 |
| Judd, KE | 1 |
| Chen, B | 1 |
| Kimura, T | 1 |
| Hosokawa-Muto, J | 1 |
| Kamatari, YO | 1 |
| Kuwata, K | 1 |
| Nguyen, T | 1 |
| Sakasegawa, Y | 1 |
| Miranda, LHL | 1 |
| Oliveira, AFPH | 1 |
| Carvalho, DM | 1 |
| Souza, GMF | 1 |
| Magalhães, JGM | 1 |
| Júnior, JAC | 1 |
| Lima, PTMBQ | 1 |
| Júnior, RMA | 1 |
| Filho, SPL | 1 |
| Melo, HMA | 1 |
| Forloni, G | 2 |
| Artuso, V | 1 |
| Roiter, I | 1 |
| Morbin, M | 1 |
| Tagliavini, F | 2 |
| Bian, J | 1 |
| Kang, HE | 1 |
| Telling, GC | 1 |
| Tsuboi, Y | 2 |
| Šafařík, M | 1 |
| Moško, T | 1 |
| Zawada, Z | 1 |
| Šafaříková, E | 1 |
| Dračínský, M | 1 |
| Holada, K | 1 |
| Šebestík, J | 1 |
| Spilman, P | 1 |
| Lessard, P | 3 |
| Sattavat, M | 1 |
| Bush, C | 1 |
| Tousseyn, T | 1 |
| Huang, EJ | 1 |
| Giles, K | 2 |
| Golde, T | 1 |
| Das, P | 1 |
| Fauq, A | 1 |
| Prusiner, SB | 5 |
| Dearmond, SJ | 3 |
| Geschwind, MD | 1 |
| Collinge, J | 2 |
| Gorham, M | 1 |
| Hudson, F | 2 |
| Kennedy, A | 2 |
| Keogh, G | 1 |
| Pal, S | 1 |
| Rossor, M | 1 |
| Rudge, P | 2 |
| Siddique, D | 1 |
| Spyer, M | 1 |
| Thomas, D | 1 |
| Walker, S | 1 |
| Webb, T | 1 |
| Wroe, S | 2 |
| Darbyshire, J | 1 |
| Mangels, C | 1 |
| Frank, AO | 1 |
| Ziegler, J | 1 |
| Klingenstein, R | 1 |
| Schweimer, K | 1 |
| Willbold, D | 1 |
| Korth, C | 2 |
| Rösch, P | 1 |
| Schwarzinger, S | 1 |
| Puopolo, M | 1 |
| Pocchiari, M | 1 |
| Petrini, C | 1 |
| Sakaguchi, S | 1 |
| Sasvari, Z | 1 |
| Bach, S | 1 |
| Blondel, M | 1 |
| Nagy, PD | 1 |
| Ghaemmaghami, S | 1 |
| Ahn, M | 2 |
| Legname, G | 2 |
| Mead, S | 1 |
| Ranopa, M | 1 |
| Gopalakrishnan, GS | 1 |
| Thompson, AG | 1 |
| MacKay, A | 1 |
| Darbyshire, JH | 1 |
| Walker, AS | 1 |
| Bajsarowicz, K | 1 |
| Ackerman, L | 1 |
| Dearmond, BN | 1 |
| Carlson, G | 1 |
| Mays, CE | 1 |
| Joy, S | 1 |
| Li, L | 1 |
| Yu, L | 1 |
| Genovesi, S | 1 |
| West, FG | 1 |
| Westaway, D | 1 |
| Caughey, B | 1 |
| Baron, GS | 1 |
| May, BC | 2 |
| Fafarman, AT | 1 |
| Hong, SB | 1 |
| Rogers, M | 1 |
| Deady, LW | 1 |
| Cohen, FE | 2 |
| Barret, A | 1 |
| Bate, C | 1 |
| Salmona, M | 1 |
| Colombo, L | 1 |
| De Luigi, A | 1 |
| Limido, L | 1 |
| Suardi, S | 1 |
| Rossi, G | 1 |
| Auvré, F | 1 |
| Adjou, KT | 1 |
| Salès, N | 1 |
| Williams, A | 1 |
| Lasmézas, C | 1 |
| Deslys, JP | 1 |
| Murakami-Kubo, I | 1 |
| Ishikawa, K | 1 |
| Kawatake, S | 1 |
| Sasaki, K | 1 |
| Kira, J | 1 |
| Ohta, S | 1 |
| Iwaki, T | 1 |
| Dohgu, S | 1 |
| Yamauchi, A | 1 |
| Takata, F | 1 |
| Sawada, Y | 1 |
| Higuchi, S | 1 |
| Naito, M | 2 |
| Tsuruo, T | 2 |
| Shirabe, S | 1 |
| Niwa, M | 1 |
| Katamine, S | 1 |
| Kataoka, Y | 2 |
| Yung, L | 1 |
| Huang, Y | 1 |
| Lin, ET | 1 |
| Baldwin, M | 1 |
| Ryou, C | 1 |
| Guglielmo, BJ | 1 |
| Gayrard, V | 1 |
| Picard-Hagen, N | 1 |
| Viguié, C | 1 |
| Laroute, V | 1 |
| Andréoletti, O | 1 |
| Toutain, PL | 1 |
| Tamura, K | 1 |
| Karube, Y | 1 |
| Mayer-Sonnenfeld, T | 1 |
| Avrahami, D | 1 |
| Friedman-Levi, Y | 1 |
| Gabizon, R | 1 |
| Love, R | 1 |
| Stewart, LR | 1 |
| White, AR | 1 |
| Jobling, MF | 1 |
| Needham, BE | 1 |
| Maher, F | 1 |
| Thyer, J | 1 |
| Beyreuther, K | 1 |
| Masters, CL | 1 |
| Collins, SJ | 1 |
| Cappai, R | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Novel Therapeutics For Prion Diseases: A Randomized, Double-blinded, Placebo-controlled Study of the Efficacy of Quinacrine in the Treatment of Sporadic Creutzfeldt-Jakob Disease[NCT00183092] | Phase 2 | 69 participants (Actual) | Interventional | 2005-04-30 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
"Verbal fluency tests are a kind of psychological test in which participants have to say as many words as possible from a category in 60 seconds. This category (words beginning with letter D) is phonemic. Higher scores indicate better cognition." (NCT00183092)
Timeframe: Baseline, 2 months
| Intervention | number of words generated (Mean) |
|---|---|
| Placebo | -2.4 |
| Quinacrine | -2.2 |
ADAS-cog measures cognitive performance by combining ratings of 11 components (word recall, word recognition, constructional praxis, orientation, naming objects and fingers, commands, ideational praxis, remembering instruction, spoken language, word finding, comprehension) representing six areas of cognition: memory; language; orientation to time, place and person; construction of simple designs and planning; and performing simple behaviors in pursuit of a basic, predefined goal. Seven components are scored as the 'number incorrect'. For example, in the commands component, the number of five commands performed incorrectly (range: 0-5). Four components are scored from 0 (no limitations) to 5 (max limitations) as the examiner's perception of remembering instructions, spoken language ability, word finding and comprehension. Component scores are summed into a total ADAS-cog score ranging from 0-75, with low scores indicating better cognitive performance. (NCT00183092)
Timeframe: Baseline, 2 months
| Intervention | units on a scale (Mean) |
|---|---|
| Placebo | 13.0 |
| Quinacrine | 12.6 |
An ordinal scale used to measure performance in activities of daily living. Scores range from 0 (worst, fully dependent) to 100 (best, independent); higher score associated with a greater likelihood of being able to live at home with a degree of independence following discharge from hospital. 10 individual items are scored and summed to derive the overall Barthel index score. Each item may be scored 0, 5, 10 or 15; not all items use the full range of 4 possible values. The amount of time and physical assistance required to perform each item are considered in scoring each item. For subjects unable to return for month-2 visit, Barthel Index was performed via telephone. (NCT00183092)
Timeframe: baseline, 2 months
| Intervention | units on a scale (Mean) |
|---|---|
| Placebo | -23.2 |
| Quinacrine | -13.2 |
Clinical Dementia Rating Scale Sum of Boxes (CDRS-SB). The CDR is obtained through semistructured interviews of patients and informants, and cognitive functioning is rated in 6 domains of functioning: memory, orientation, judgment and problem solving, community affairs, home and hobbies, and personal care. Each domain is rated on a 5-point scale of functioning: 0, no impairment; 0.5, questionable impairment; 1, mild impairment; 2, moderate impairment; and 3, severe impairment (personal care is scored on a 4-point scale without a 0.5 rating available). The global CDR score is computed via an algorithm. The CDR-SB score is obtained by summing each of the domain box scores, with scores ranging from 0 to 18. A higher value and/or positive change is worse. For subjects unable to return for month-2 visit, CDRS-SB was performed via telephone. (NCT00183092)
Timeframe: Baseline, 2 months
| Intervention | units on a scale (Mean) |
|---|---|
| Placebo | 3.2 |
| Quinacrine | 0.3 |
The mini-mental state examination (MMSE) is a brief 30-point questionnaire that is used to screen for cognitive impairment. In about 10 minutes it samples functions including arithmetic, memory and orientation. A score greater than or equal to 25 points (out of 30) indicates a normal cognition. Lower scores can indicate severe (≤9 points), moderate (10-18 points) or mild (19-24 points) cognitive impairment. Low to very low scores correlate closely with the presence of dementia, although other mental disorders can also lead to abnormal findings on MMSE testing. (NCT00183092)
Timeframe: Baseline to Month-2
| Intervention | units on a scale (Mean) |
|---|---|
| Placebo | -6.9 |
| Quinacrine | -3.9 |
"The scale runs from 0-6, running from perfect health without symptoms to death. 0 - No symptoms.~- No significant disability. Able to carry out all usual activities, despite some symptoms.~- Slight disability. Able to look after own affairs without assistance, but unable to carry out all previous activities.~- Moderate disability. Requires some help, but able to walk unassisted.~- Moderately severe disability. Unable to attend to own bodily needs without assistance, and unable to walk unassisted.~- Severe disability. Requires constant nursing care and attention, bedridden, incontinent.~- Dead. For subjects unable to return for the 2-month visit, Rankin score was assessed via telephone." (NCT00183092)
Timeframe: Baseline, 2 months
| Intervention | units on a scale (Mean) |
|---|---|
| Placebo | 0.8 |
| Quinacrine | 0.3 |
Verbal fluency tests are a kind of psychological test in which participants have to say as many words as possible from a category in 60 seconds. This category (naming animals) is semantic. Higher scores indicate better cognition. (NCT00183092)
Timeframe: Baseline, 2 months
| Intervention | number of words generated (Mean) |
|---|---|
| Placebo | -3.2 |
| Quinacrine | -2.2 |
Participants alive after 2 months on study treatment (NCT00183092)
Timeframe: Randomization to Month-2
| Intervention | participants (Number) |
|---|---|
| Placebo | 19 |
| Quinacrine | 13 |
4 reviews available for quinacrine and Dementias, Transmissible
| Article | Year |
|---|---|
Systematic review of pharmacological management in Creutzfeldt-Jakob disease: no options so far?
Topics: Aminopyridines; Creutzfeldt-Jakob Syndrome; Doxycycline; Humans; Pentosan Sulfuric Polyester; Prion | 2022 |
Therapy in prion diseases.
Topics: Animals; Doxycycline; Humans; Pentosan Sulfuric Polyester; Prion Diseases; Prions; Quinacrine | 2013 |
[Systematic review of the therapeutics for prion diseases].
Topics: Aminopyridines; Animals; Antibodies, Monoclonal; Blood-Brain Barrier; Brain; Cattle; Clinical Trials | 2009 |
[Therapeutics for prion diseases].
Topics: Amyloid; Animals; Benzothiazoles; Clinical Trials as Topic; Drug Design; Humans; Pentosan Sulfuric P | 2003 |
2 trials available for quinacrine and Dementias, Transmissible
| Article | Year |
|---|---|
Safety and efficacy of quinacrine in human prion disease (PRION-1 study): a patient-preference trial.
Topics: Adolescent; Adult; Age Factors; Aged; Aged, 80 and over; Female; Follow-Up Studies; Humans; Kaplan-M | 2009 |
A possible pharmacological explanation for quinacrine failure to treat prion diseases: pharmacokinetic investigations in a ovine model of scrapie.
Topics: Algorithms; Animals; Cell Line, Tumor; Culture Media; Extracellular Space; Female; Injections, Intra | 2005 |
28 other studies available for quinacrine and Dementias, Transmissible
| Article | Year |
|---|---|
Antiprion activity of functionalized 9-aminoacridines related to quinacrine.
Topics: Aminoacridines; Cell Line; Humans; Prion Diseases; Prions; Quinacrine; Structure-Activity Relationsh | 2008 |
Design, synthesis, and structure-activity relationship of indole-3-glyoxylamide libraries possessing highly potent activity in a cell line model of prion disease.
Topics: Amides; Amines; Animals; Cell Line; Drug Design; Indoles; Mice; Prion Diseases; Small Molecule Libra | 2009 |
Synthesis of GN8 derivatives and evaluation of their antiprion activity in TSE-infected cells.
Topics: Acetanilides; Animals; Antiparasitic Agents; Benzhydryl Compounds; Inhibitory Concentration 50; Mice | 2011 |
Anti-prion activities and drug-like potential of functionalized quinacrine analogs with basic phenyl residues at the 9-amino position.
Topics: Animals; ATP Binding Cassette Transporter, Subfamily B, Member 1; Binding Sites; Biological Transpor | 2011 |
Quinacrine promotes replication and conformational mutation of chronic wasting disease prions.
Topics: Animals; Cell Line; Cell Survival; Deer; Humans; Mice; Mutation; Prion Diseases; Prions; Protein Con | 2014 |
[Current Trends in the Treatment of Prion Disease].
Topics: Clinical Trials as Topic; Humans; Prion Diseases; Prions; Prognosis; Quinacrine | 2015 |
Reactivity of 9-aminoacridine drug quinacrine with glutathione limits its antiprion activity.
Topics: Biological Availability; Drug Evaluation; Glutathione; Humans; Hydrophobic and Hydrophilic Interacti | 2017 |
A gamma-secretase inhibitor and quinacrine reduce prions and prevent dendritic degeneration in murine brains.
Topics: Administration, Oral; Alanine; Amyloid Precursor Protein Secretases; Animals; Azepines; Brain; Dendr | 2008 |
Clinical trials for prion disease: difficult challenges, but hope for the future.
Topics: Aminopyridines; Clinical Trials as Topic; Humans; Prion Diseases; Quinacrine; Randomized Controlled | 2009 |
Binding of TCA to the prion protein: mechanism, implication for therapy, and application as probe for complex formation of bio-macromolecules.
Topics: Aminacrine; Animals; Humans; Models, Molecular; Molecular Probes; Molecular Structure; Nuclear Magne | 2009 |
Clinical trials and methodological problems in prion diseases.
Topics: Clinical Trials as Topic; Data Interpretation, Statistical; Drug Approval; Enzyme Inhibitors; Humans | 2009 |
Inhibition of RNA recruitment and replication of an RNA virus by acridine derivatives with known anti-prion activities.
Topics: Acridines; Antiviral Agents; Chemistry, Pharmaceutical; Chlorpromazine; Drug Design; Models, Genetic | 2009 |
Continuous quinacrine treatment results in the formation of drug-resistant prions.
Topics: Animals; ATP Binding Cassette Transporter, Subfamily B; ATP-Binding Cassette Sub-Family B Member 4; | 2009 |
PRION-1 scales analysis supports use of functional outcome measures in prion disease.
Topics: Adult; Aged; Antimalarials; Female; Follow-Up Studies; Humans; Male; Middle Aged; Neuropsychological | 2011 |
A brain aggregate model gives new insights into the pathobiology and treatment of prion diseases.
Topics: Alanine; Animals; Azepines; Brain; Cathepsin D; Dendrites; Disease Models, Animal; Embryo, Mammalian | 2012 |
Prion inhibition with multivalent PrPSc binding compounds.
Topics: Animals; Cell Line, Tumor; Chloroquinolinols; Congo Red; Humans; Inhibitory Concentration 50; Mice; | 2012 |
[Development of therapeutic interventions for prion disease].
Topics: Humans; Pentosan Sulfuric Polyester; Prion Diseases; Quinacrine | 2012 |
Factors affecting interactions between prion protein isoforms.
Topics: Animals; Cattle; Goats; Humans; Prion Diseases; Prions; Protease Inhibitors; Protein Conformation; P | 2002 |
Potent inhibition of scrapie prion replication in cultured cells by bis-acridines.
Topics: Acridines; Animals; Cell Line; Drug Evaluation, Preclinical; Humans; Mice; Prion Diseases; PrPSc Pro | 2003 |
Evaluation of quinacrine treatment for prion diseases.
Topics: Animals; Chlorpromazine; Cricetinae; Drug Resistance; Endopeptidase K; Humans; Melatonin; Mice; Mice | 2003 |
Quinoline derivatives are therapeutic candidates for transmissible spongiform encephalopathies.
Topics: Animals; Brain; Humans; Immunohistochemistry; Injections, Intraventricular; Mice; Mice, Transgenic; | 2004 |
Uptake and efflux of quinacrine, a candidate for the treatment of prion diseases, at the blood-brain barrier.
Topics: Animals; ATP Binding Cassette Transporter, Subfamily B, Member 1; Blood-Brain Barrier; Cation Transp | 2004 |
Pharmacokinetics of quinacrine in the treatment of prion disease.
Topics: Administration, Oral; Animals; Brain; Chromatography, High Pressure Liquid; Disease Models, Animal; | 2004 |
Chelating compound, chrysoidine, is more effective in both antiprion activity and brain endothelial permeability than quinacrine.
Topics: Animals; Brain; Cell Membrane Permeability; Chelating Agents; Drug Evaluation, Preclinical; Endothel | 2007 |
Chemically induced accumulation of GAGs delays PrP(Sc) clearance but prolongs prion disease incubation time.
Topics: Animals; Antiviral Agents; Central Nervous System; CHO Cells; Cricetinae; Cricetulus; Enzyme Inhibit | 2008 |
Acridine and phenothiazine derivatives as pharmacotherapeutics for prion disease.
Topics: Acridines; Animals; Cells, Cultured; Chlorpromazine; Fatty Acids; Humans; Mice; Neuroblastoma; Pheno | 2001 |
Old drugs to treat new variant Creutzfeldt-Jakob disease.
Topics: Animals; Antimalarials; Antipsychotic Agents; Chlorpromazine; Creutzfeldt-Jakob Syndrome; Drug Thera | 2001 |
Involvement of the 5-lipoxygenase pathway in the neurotoxicity of the prion peptide PrP106-126.
Topics: Animals; Annexin A5; Anti-Inflammatory Agents, Non-Steroidal; Arachidonate 5-Lipoxygenase; Arachidon | 2001 |