The major effect of cholinesterase inhibitors, which remains to be confirmed in prospective longitudinal clinical trials, lies in their potential to slow the rate of progression of Alzheimer disease. One retrospective analysis suggested that long-term use of donepezil may slow the rate of disease progression 106 ; . If slowed progression is verified in clinical trials under way in the United States, the drug might be indicated, even in the absence of observable improvement in cognition or function. To date, only highdose vitamin E has been shown to have this effect. In a multi-institutional, double-blind, placebo-controlled prospective study, 341 moderately impaired patients Clinical Dementia Rating score, 2 ; were randomly assigned to receive 2000 IU of vitamin E, 10 mg of selegiline, vitamin E and selegiline, or placebo for 2 years. The primary end point was the time to progression to any of the following end points: death, institutionalization, loss of any two of three basic activities of daily living eating, dressing, and toileting ; , or a rating of 3 on the Clinical Dementia Rating Scale. Using an intention-to-treat analysis and after adjustment for differences among the groups in the baseline Mini-Mental State Examination score, the investigators found a significant delay in the primary outcome among the treatment groups increase in median survival of 230 days for patients taking vitamin E, 215 days for patients taking selegiline, and 145 days for patients taking vitamin E and selegiline ; compared with placebo recipients 101 ; . The interpretation was somewhat controversial because of the need to include the baseline Mini-Mental State Examination score as a covariant in order to demonstrate a statistically significant difference between the treatment and placebo groups. Nevertheless, the American Academy of Neurology now recommends 1000 IU of vitamin E twice daily as a standard care for the treatment of patients with Alzheimer disease 105 ; . The effectiveness of anti-inflammatory drugs in slowing the progression of Alzheimer disease remains controversial. A single trial using low-dose prednisone showed no benefit 107 ; . Initial reports from a study using a nonspecific cyclooxygenase inhibitor indomethacin ; suggested some benefit; however, 40% of the participants receiving the active medication dropped out of the study, mainly as a result of gastrointestinal toxicity 108 ; . Trials using the newer cyclooxygenase-2 inhibitors have also been disappointing. Although several casecontrol and cohort studies 109 114 ; suggest that postmenopausal women who used estrogen replacement therapy had a reduced risk for Alzheimer disease, other studies have not confirmed this find406 4 March 2003 Annals of Internal Medicine Volume 138 Number 5 and hytrin.

Monoamine oxidase type B inhibitors MAOBIs ; have been used since the mid-1970s to treat the symptoms of Parkinson's disease PD ; , presumably by lessening oxidative stress and enhancing the effect of dopamine. In this article, I will discuss three different MAOBIs in terms of their effectiveness as symptomatic therapies: selegiline, zydis-selegiline, and rasagiline, which has recently been approved in Europe and the United States. Zelegiline Europe ; and rasagiline Europe and US ; are approved as monotherapy for patients in the early stages of the disease. Selegiline, zydis-selegiline and rasagiline are approved for use as adjunct to levodopa in patients with motor fluctuations who have progressed to more advanced stages. The monoamine oxidases are enzymes that deaminate, oxidize, and eliminate the activity of monoamines, including dopamine, serotonin, and norepinephrine. Inhibitors of these enzymes thus increase levels of these important neurotransmitters and have been used since the 1950s to treat depression, although they have been largely replaced as depression treatments by more recently developed drugs such as the tricyclics and selective serotonin reuptake inhibitors SSRIs ; . Monoamine oxidase inhibitors exist in two forms, A and B, distinct enzymes that are encoded by different genes, act on different substrates, and are found in different tissues, with some overlap. Monoamine oxidase type A inhibitors MAOAIs ; , but not MAOBIs, cause what is called "the cheese effect, " which can lead to hypertensive crisis if the person taking the drug ingests foods with high levels of tyramine, such as tap beers, processed meats or aged cheese. The reason for this is that MAO-As, found predominantly in the gut, portal system, and adrenergic neurons, facilitate the metabolism of tyramine to inactive substances. Inhibition of MAO-As results in increased levels of tyramine, which can precipitate the release of noradrenaline from sympathetic neurons in the circulatory system 1. MAOBIs do not cause the "cheese effect, " when they are used at doses that remain relatively specific to MAO-B and are therefore considered safer than MAOAIs. At these therapeutic doses, they do not require diet restrictions in Europe, no tyramine diet restriction is recommended for the use of rasagiline, while this is presently the case in the US ; . However, at higher doses, all MAO-B inhibitor loose specificity for MAO-B. They can therefore block MAO-A and induce cardiovascular adverse reactions. Selegilihe and rasagiline irreversibly block MAO-Bs2, such that MAO-B activity will not return to normal until the body has had time to resynthesize the enzyme. For rasagiline, this requires at least 32 days. The two drugs have different metabolites: Eelegiline is metabolized into amphetamine-like compounds, which may lead to adverse reactions including cardiovascular effects; while the primary metabolite of rasagiline is a compound known as aminoindan, which does not cause cardiovascular problems and may be involved in.

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