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Regarding “New Therapies in the Pipeline for AD — What's Promising, What's Not” (Sept. 4), the information on treatment of Alzheimer disease (AD) with methylthionium chloride or MTC, was especially encouraging since it prevented loss of brain volume, and slowed the rate of decline 81 percent when compared to placebo at 24 weeks in AD patients — a favorable result when compared to currently available treatments.

MTC is also known as methylene blue, which has been used for numerous conditions for over a century, including the first treatment for malaria and urinary tract infections. It is even used as an antiseptic for fish-tanks and aquariums.

While methylene blue interferes with the aggregation of tau fibers which aggregrate in AD, it also enhances mitochondrial function, which is markedly impaired in AD.

Besides inhibiting tau aggregation, mitochondrial dysfunction in AD may be another target for treatment, which methylene blue may reverse.

If an old medicine such as methylene blue, which has been around for more than a century and is thought to be quite safe, is found to offer substantial benefit in AD, then I don't see any reason to delay treatment. The disease is uniformly fatal, no one having recovered as yet, and is devastating as it advances.

Current treatments, such as acetycholinesterase inhibitors, delay progression but only offer a temporary respite, and don't have disease-modifying effect. Other diseases having mitochondrial connections such as Parkinson disease, ALS, and temporal lobe epilepsy with Ammon's horn sclerosis might have some potential for treatment as well.

Hopefully quick progress will be made in accelerating studies involving the treatment of AD if a treatment such as methylene blue comes along, rather than continuing on with “business as usual.”

Steven Brenner, MD

St. Louis VA Medical Center, Department of Neurology and Psychiatry, St. Louis, MO


• Atamna H, Nguyen A, Newberry J, et al. Methylene blue delays cellular senescence and enhances key mitochondrial biochemical pathways. FASEB Journal 2008;22:701–712.
    • Devi L, Prabhu BM, Anandatheerthavarada HK, et al. Accumulation of amyloid precursor protein in the mitochondrial import channels of Alzheimer's disease brain is associated with mitochondrial dysfunction. J Neurosci 2006;26(35):9057–9068.
      • Baron M, Kudin AP, Kunz WS, Mitochondrial dysfunction in neurodegenerative disorders. Biochem Soc Trans 2007; 35(pt 5):1228–1231.