Two new studies indicate potential benefits for Alzheimer's patients. One found that Lipitor, a cholesterol-lowering medication, slows the progression of Alzheimer's disease while another found that an anti-inflammatory drug slowed plaque deposits in mice.
Participants in a one-year treatment trial received either Lipitor or a placebo. A total of two-thirds of the patients on active medication derived some clinical benefit. Half of the patients stabilized or actually improved, according to D. Larry Sparks, Ph.D., a senior scientist at the Sun Health Research Institute in Arizona.
"This is truly exciting news," Dr. Sparks exclaims. "Results indicate not only a slowing in deterioration of function and memory but also an improvement in mood and behavior. No prior clinical trials have actually shown long-term improvement in patients with AD."
Other studies have also suggested that cholesterol may exacerbate the progression of Alzheimer's disease, leading researchers to speculate that Lipitor and other statins might protect against further deterioration in Alzheimer's patients.
In Sparks' study, participants were not excluded from medications they already were taking for pre-existing conditions. Results indicate Lipitor was effective regardless of other medications already being taken.
In addition to this trial, Dr. Sparks also is participating in the ongoing LEADe study sponsored by Pfizer, Inc., which is comparing the efficacy and safety of Lipitor in combination with donepezil (Aricept) in a large group of patients with mild to moderate AD.
Sparks' AD Cholesterol-lowering Treatment Trial was the first clinical trial of its kind designed to test the clinical benefits of atorvastatin (Lipitor) in both memory and behavioral measures. The study received initial support from the Institute for the Study on Aging (ISOA), which awarded Sparks a $450,000 grant. Additional funding came from Pfizer Pharmaceutical, Inc., which also supplied Lipitor and placebo for the study.
Anti-Inflammatory
Meanwhile, Finnish researchers said a derivative of flurbiprofen was found to significantly reduce beta-amyloid deposition in the brain of a mouse model of Alzheimer's disease.
The study was conducted by Dr. Thomas van Groen and his group at the University of Kuopio, Finland, who have conducted long-standing experiments on mice bred to be predisposed to develop deposits of beta-amyloid, a key hallmark of Alzheimer's Disease.
HCT 1026 was administered as part of the diet for a period of six months, starting at eight months of age, prior to plaque formation. Treatment with HCT 1026 produced a significant decrease in beta-amyloid deposition in the dorsal hippocampus, an important area for cognitive function which is primarily affected by beta-amyloid deposits early in the disease process. The effects were significant for both diffuse and dense plaques.
The beta-amyloid deposits were reduced in size and had fewer inflammatory markers surrounding them, an indicator of decreased toxicity of those amyloid deposits that were present. No signs of side effects, such as noticeable changes of behavior, were observed during the treatment period. Body weight gain, which is usually adversely affected by gastrointestinal lesions, was normal.
"These data show that long-term treatment with HCT 1026 leads to a reduction of the beta-amyloid pathology, which is a major component of Alzheimer's disease. Furthermore, HCT 1026 was very well tolerated with no signs of side effects. Overall, these results suggest that HCT 1026 may have potential in the reduction of a key pathological event in the brain of AD patients," van Groen said at a conference in France.
The research followed the decision of the steering committee of the American National Institute on Aging (NIA) Interventions Testing Program (ITP) to select HCT 1026 as one of four compounds for studies on longevity in mice. HCT 1026 was considered particularly interesting because of its well- established anti-inflammatory properties and its safety profile, which has been documented in a wide range of studies.
