Case clioquinol

There was a major epidemic of subacute myelo-optic neuropathy (SMON) in Japan during 1956-70. In 1970 a clinical observation led to case-control and cohort studies, which identified clioquinol as the culprit. A few cases were also reported elsewhere in the world, in Australia (2), Denmark (3), the Netherlands (4), Sweden (5-7), Switzerland (8), the UK (9-11), and the USA (12) some cases involved halogenated quinolines other than clioquinol. Prolonged use of diiodohydroxyquinoline in high doses has been associated with loss of vision and optic atrophy (SED-11, 594) (13). Halogenated quinolines were withdrawn in Japan and the epidemic abated (14). 

Clioquinol (CQ) was initially tested on post-mortem AD brain for its Ab solubilizing activity. These studies revealed that CQ doubled the amount of soluble Ab in brain extracts [179]. CQ was subsequently tested in APP transgenic mice (Tg2576) in a 12-week blind, controlled study [179]. An amount of 20 mg/kg daily of CQ significantly reduced the level of insoluble Ab in brain extracts. A further 9-week study (30 mg/kg daily) was performed on older mice (21 months versus 12 months in the earlier study). In this case, in-... 

Meade, T.W. (1975) Subacute myelo-optic neuropathy and clioquinol. An epidemiological case history for diagnosis. Brit. J. prev. soc. Med., 29,157. 

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