Disease Modification

Medications in this category are designed to attack the underlying neuropathological features of Alzheimer's disease, thereby halting disease progression and either preventing further symptom progression or reversing symptoms that have already been established. The most common targets of disease-modification strategies for Alzheimer's disease are the two primary neuropathological features: beta-amyloid, which forms amyloid plaques, and tau, the primary constituent of neurofibrillary tangles.

• Alzhemed. This compound is believed to work by binding to beta-amyloid while it is still in a soluble form, thereby preventing it from transitioning to the "sticky" form it assumes when it aggregates into plaques. Alzhemed also may achieve some effect through an anti-inflammatory mechanism. In a multicenter clinical trial begun in 2004, Alzhemed has shown promise in stabilizing symptoms in people with mild to moderate Alzheimer's disease.

• Clioquinol. Clioquinol (iodochlorhydroxyquin) is an old-line antibiotic that has recently shown potential promise in the treatment of Alzheimer's disease. Clioquinol appears to work by extracting metals (zinc and copper) from beta-amyloid, thereby effectively "disassembling" amyloid plaques. Clioquinol also appears to decrease the production of hydrogen peroxide, which is toxic to neurons.

• Alzheimer's disease vaccine. Traditional vaccines in humans are used to provoke the production of specialized proteins called antibodies, our natural defenses against pathogens. There is reason to believe that a vaccine can be a weapon against Alzheimer's disease. This hope was raised by the finding that the human immune system contains antibodies against beta-amyloid protein.

A 1999 landmark study reported on the development of an injectable vaccine (AN-1792), which successfully cleared Alzheimer's pathology in mice that were genetically engineered to have high levels of human brain beta-amyloid. Clinical trials initiated in 2001 with 372 humans from twenty-eight study sites were discontinued in January 2002 after four subjects developed encephalitis, a potentially fatal brain inflammatory response. Ultimately, 6 percent of the research sample developed symptoms or had other findings associated with encephalitis.

One of the people who developed encephalitis later died from an unrelated cause (pulmonary embolism). However, a brain autopsy revealed that AN-1792 had successfully cleared much of the Alzheimer's pathology in the same way as had been demonstrated in earlier animal research. Although researchers must remain cautious about drawing conclusions from a single case, this finding implies that a robust immunological response had occurred and was dramatically effective on the physiological level.

In another report, published in 2003, researchers at one of the clinical trial sites in Switzerland reported that analysis of their thirty patients suggested that immunization had slowed disease progression. Again, caution must be exercised in drawing general conclusions from these data. Nevertheless, the findings have generated a good deal of excitement and optimism, and a number of different research groups are now working on a second generation of modified "passive" immunization strategies.

• Lithium-like drugs. Long used to treat bipolar disorder (manic-depressive illness), lithium is being studied for its potential to treat Alzheimer's disease. In animal research, lithium has been found to block an enzyme (glycogen synthase kinase) that is essential to the formation of beta-amyloid plaques. Lithium also appears to interfere with the production of the tau protein, another suspected pathological feature of Alzheimer's disease.

However, even if lithium has the same beneficial effect in humans, it's doubtful that it would constitute a practical treatment for Alzheimer's disease because it can produce a number of side effects, and elderly people would be especially vulnerable to them. But other drugs might be developed that inhibit the Alzheimer's process in the same way as lithium.

• Secretase inhibitors. Gamma- and beta-secretase are enzymes that detach the beta-amyloid segment from a larger protein, effectively putting it into position to begin the process of aggregating into plaques. Compounds that inhibit these enzymes have become an intense focus of research as potential disease-modifying agents, although none have yet advanced to actual treatment studies.

• Phenserine. Phenserine is a new cholinesterase inhibitor currently in advanced clinical trials that is purported to have both symptomatic and potential disease-modifying effects, which can slow the progression of Alzheimer's disease. Researchers say that it has demonstrated the ability to inhibit formation of the amyloid precursor protein, the source of beta-amyloid.

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