Abstract

ANAHEIM, CALIF. — “Aging and Alzheimer's disease are not synonymous,” Dr. John C. Morris told attendees at the Advances in Alzheimer's session at the 2006 joint conference of the American Society on Aging and the National Council on Aging. Dr. Morris, the Friedman Distinguished Professor of Neurology at Washington University, St. Louis, contends that Alzheimer's disease (AD) is not an inevitable consequence of aging. “Truly, healthy patients have cognitive mental abilities that remain surprisingly intact,” he said. During healthy aging, an individual gets more easily distracted, cannot multitask as well, and takes longer to perform a given task, but the task is still done accurately. The prevalence of AD among Americans is 5% at age 65, and doubles for every 5 years of age over 65, according to Dr. Morris. Even so, by age 85, only 50% of the population has AD, leaving many a healthy senior. “In truly healthy aging, an individual can be quite vibrant, even to age 100,” Dr. Morris said. Dr. Morris also contends that AD is not only treatable but also preventable. Drugs that are being tested in clinical trials inhibit production or promote degradation and clearance of amyloid-β, the protein that forms plaques in AD patients' brains. “If we wanted to stop AD, we have the potential candidates. All we need to do is evaluate them to find out which are safe and effective,” Dr. Morris stated. AD is both underdiagnosed and undertreated. Of approximately 4.5 million Americans diagnosed with AD, only 2.8 million (62%) have received a definite diagnosis. Of those, only half are being treated with cholinesterase inhibitors (ChEIs). By the time AD patients are diagnosed, on average, 60% of their brain cells already are damaged, Dr. Morris said. He added that that justifies use of prophylactic treatment in individuals with mild cognitive impairment (MCI), who are at high risk of Alzheimer's. According to the guidelines of the American Academy of Neurology (Neurology 2001;56:1154–66), ChEIs such as donepezil (Aricept) are the standard treatment for dementia, and high-dose vitamin E is recommended. Newer drugs, such as memantine (Namenda), also are useful. Dr. Morris said ChEIs are cost effective for patients with MCI; although the drugs are not a cure, they can slow dementia or help patients maintain their mental functioning. Another preventive approach would be to develop an AD vaccine. Dr. James A.R. Nicoll and colleagues tested an AD vaccine in a single patient and compared the response to seven control subjects (Nat. Med. 2003;9:448–52). Based on in vivo imaging, the vaccine apparently cleared amyloid-β from the brain of the immunized participant, but Dr. Morris said there was no evidence that the vaccine benefited the patient clinically. He described one cutting-edge diagnostic technique using Pittsburgh compound B (PIB), a PET tracer used for in vivo imaging of amyloid-β plaques (Ann. Neurol. 2004;55:306–19). In 9 of 10 individuals with AD, the PIB binding potential was consistently higher than in healthy controls. PIB binding and CSF amyloid-β concentrations corresponded to clinical diagnosis of Alzheimer's (Ann. Neurol. 2006;59:512–9). Investigators have identified certain biomarkers in patients with MCI that may predict AD development using a variety of techniques (amyloid-βconcentrations in blood plasma, neuroimaging, functional imaging with functional MRI, PET, or single-photon emission computed tomography). “Increasingly, we are able to detect the subset of patients with mild cognitive impairment who will progress to AD,” Dr. Morris said.

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