The homocysteine pathway: A new target for Alzheimer disease treatment?

José I. Lao, Katrin Beyer, Aurelio Ariza

Research output: Contribution to journalReview articleResearchpeer-review

4 Citations (Scopus)


One of the known risk factors for developing Alzheimer disease (AD) is hyperhomocysteinemia. The latter may result from mutations of the genes coding for three key enzymes involved in homocysteine metabolism (methylenetetrahydrofolate reductase [MTHFR], methionine synthase [MS], and cystathionine beta-synthase [CBS]). Polymorphisms within the three genes have been shown to be positively associated with AD in some populations. Whereas MS and MTHFR polymorphisms have been described as AD risk factors independently on age at onset of the disease, two of the CBS polymorphisms were found to depend on age at onset of AD. The division of AD patients and controls into age-at-onset/ age dependent subgroups (<65 years, 65-74 years, ≥75 years) revealed that the 844ins68 mutation and variable number of tandem repeats allele 19 are independent risk factors for AD development in subjects aged 75 years or more. Although homocysteine levels can be regulated by dietary intake of folic acid, B vitamins, and other components, the genotype-dependent design of strategies for the maintenance of adequate homocysteine levels could be helpful for AD treatment. In addition to each specific genotype, age and age at onset of AD are important factors for specific regulation of the homocysteine metabolism. One of the molecules to take into account in the case of AD is choline, which serves as methyl-group donor when MS activity is impaired. © 2004 Wiley-Liss, Inc.
Original languageEnglish
Pages (from-to)221-230
JournalDrug Development Research
Issue number3
Publication statusPublished - 1 Jul 2004


  • Alzheimer disease
  • Cystathionine beta synthase
  • Homocysteine
  • Methionine synthase
  • Treatment


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