van Riemsdijk MM, et al. “Neuropsychiatric events during prophylactic use of mefloquine before travelling”, Published online: 27 July 2002, Springer-Verlag
MASTA (Malaria Advisory Services for Travelles Abroad) study: Comparison of adverse events associated with use of mefloquine and combination of chloroquine and proguanil as antimalarial prophylaxis: postal and telephone survey of travellers P J Barrett, P D Emmins, P D Clarke, D J Bradley, BMJ, 7056, Vol 313, August 31, 1996.
“Effectiveness of antimalarial drugs” (scroll to letter #3), Croft, Beer, Herxheimer, New England Journal of Medicine, Nov 28, 2005.
New study will examine Mefloquine as a Treatment for Malignant Glioma (Brain Cancer). Mefloquine is designed to block a protein that helps to clean the waste in the cells and to destabilize the cell membrane. Blocking this protein may cause tumor cell death. (Study registered in September 2011)
Mefloquine damage vestibular hair cells in organotypic cultures. Yu et al, Neurotox Res, July 2011.
Plasmodium falciparum Infection during Suppressive Prophylaxis with Mefloquine Does Not Induce an Antibody Response to Merozoite Surface Protein-1(42). Moon et al, Am J of Tropical Medicine and Hygiene, 2011.
Characterization of in vivo metabolites of WR319691, a novel compound with activity against Plasmodium falciparum. Milner et al, Eur J Drug Metab Pharmacokinet, 2011.
An Outbreak of Plasmodium falciparum Malaria in U.S. Marines Deployed to Liberia. Whitman et al, Am J of Tropical Medicine and Hygiene, 2010.
Mefloquine induces oxidative stress and neurodegeneration in primary rat cortical neurons. Hood et al, Neurotoxicology, 2010.
Effectiveness of malaria chemoprophylaxis against P.falciparum infection in UK travellers: Retrospective observational data. Zuckerman, Batty, Jones. Travel Med and Infectious Disease, Sept 2009.
Mefloquine neurotoxicity: A literature reveiw, Stephen Toovey, Travel Medicine and Infectious Disease, January 2009.
“Given that such individuals will not be ill on departure, and that anti-malria use is prophylactic, the prescribed agent should enjoy a very low risk-benefit ratio, i.e. prophylactic antimalarials should be very well tolerated.”
MDR1 gene polymorphisms are associated with neuropsychiatric adverse effects of mefloquine. Aarnoudse AL, van Schaik RH, Dieleman J, Molokhia M, van Riemsdijk MM, Ligthelm RJ, Overbosch D, van der Heiden IP, Stricker BH. Clinical Pharmaclogy Therapy, Oct 2006.
Mefloquine Induces Dose-Related Neurological Effects in a Rat Model. GS Dow et al., Walter Reed Army Institute of Medical Research (WRAIR), March 2006. This study documents that at treatment levels, the concentration of mefloquine in the bloodstream (reached in women after the 4th or 5th preventive dose) “caused degeneration of specific brain stem nuclei.” Also see Dow’s earlier research (below) which further documents mefloquine’s neurotoxicity.
Malaria drug blocks brain conduits. Brown University Press Release. Brown researchers have discovered that mefloquine, an anti-malarial drug, blocks two gap junction proteins, or connexins, in low doses and with very few side effects in the brains of laboratory mice. The work opens an important door: Connexins found in high concentrations in the brain are believed to play a critical role in movement, vision and memory. August 7, 2004. Study follows.
World Health Organization (WHO) report: Central Nervous System Reactions Related to the Antimalarial Drug, Mefloquine, Report from Geneva, 17 July 1989; includes list of participants.