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Hypothesis on the pathogenesis of vacuolar myelopathy, dementia, and peripheral neuropathy in AIDS
  1. ALESSANDRO DI ROCCO,
  2. PETER WERNER
  1. Department of Neurology, Beth Israel Medical Center and Albert Einstein College of Medicine
  2. New York, USA
  1. Dr A Di Rocco, Beth Israel Medical Center, PACC, 10 Union Square east, Department of Neurology, New York, NY 10003, USA.

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We read with extreme interest the article by Tan and Guiloff.1 The excellent review illustrates the current knowledge on transmethylation abnormalities in the pathogenesis of neurological complications of HIV infection. It is most convincing in its ability to bridge evidence of cytokine activation, myelinotoxic, and neurotoxic events, with abnormalities of methylation in the nervous system.

Our group has been working for years on the hypothesis that AIDS associated myelopathy and other HIV related neurological disorders are consequent to an induced metabolic abnormality of the transmethylation pathway. Our initial clinical studies with methionine supplementation suggest that signs and symptoms of myelopathy and cognitive function improve with methionine supplementation.2-5 Although still preliminary, these data offer further argument for a pathogenetic role of methylation in neurological complications of AIDS, and suggest that a therapeutic approach aimed at correcting this metabolic abnormality may be beneficial. We are now conducted a larger, controlled study to further assess treatment of neurological complications of AIDS with L-methionine.

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