Steps taken toward improving dementia treatment during 2002

In keeping with the theme of this issue of Geriatric Nursing , this column presents an overview of research findings from 2002 related to drugs that have been approved or are in development for the treatment or prevention of dementia. The sidebar summarizes research highlights, which are categorized according to their impact on progress toward the goal of advancing drug therapies for dementia.

Although 2002 was the first year since 1999 in which the Food and Drug Administration did not approve any new drugs for dementia, new and valuable information about cholinesterase inhibitors emerged from studies. Since the 1990s, clinical trials of cholinesterase inhibitors, the only drugs approved for treatment of Alzheimer disease (AD), have shown moderate improvement in cognitive, behavioral, and functional deficits associated with mild to moderate AD. Studies published during 2002 expanded our knowledge about differing and longer-term effects of three of the four approved drugs: tacrine (Cognex), donepezil (Aricept), rivastigmine (Exelon), and galantamine (Reminyl). No studies of tacrine, the first cholinesterase inhibitor, were published in 2002, and the more recently developed drugs have largely replaced it. Current studies are addressing the use of cholinesterase inhibitors in types of dementia other than AD (eg, vascular and Lewy body).

Probably the most exciting area of research on drugs for dementia is the potential role of statins (HMGCoA reductase inhibitors), drugs already widely used for hyperlipidemia. Epidemiological studies indicate that statins may be effective in preventing and treating dementia, and additional studies are in progress to explore the potential of these drugs. Studies also are underway to explore the relationship between statin drugs and pathological processes that cause dementia. One theory is that statins decrease beta-amyloid by decreasing the cholesterol burden and improving endothelial function and microvascular flow.1 However, another study2 concluded that clinical doses of statins do not significantly affect beta-amyloid secretion, but other effects of these drugs may be responsible for protecting against dementia.

For several years, researchers have been addressing questions about the inflammatory process as a causative factor in dementia, and pharmaceutical companies have been particularly interested in the potential role of anti-inflammatory drugs for preventing or treating dementia. Studies published during 2002 do not support the use of these drugs for treatment, but they indicate that there may be a role for anti-inflammatory drugs in dementia prevention. In addition, researchers continued to focus on the development of new types of drugs for dementia and safe and effective drugs to manage dementia-related behaviors.

This column would be remiss if it did not mention the major recent disappointment associated with the cessation of clinical trials of the human beta-amyloid vaccine for AD because some participants developed meningoencephalitis. Despite this step backward and a few other disappointments, 2002 heralded much new information leading to developments in both prevention and treatment of dementia, and hope still hovers on the horizon.