Normal Cognitive Aging, Cognitive Decline, and AD: What's the Difference?

As knowledge grows about normal cognitive aging, AD, and the stages in between, it is increasingly evident that there is no clear line between a completely healthy brain and a diseased brain. Evidence shows that most people develop some plaques and tangles in their brains as they get older, but not everyone develops cognitive problems, amnestic MCI, or AD. At what point does an age-related process become a disease-causing process? Several recent studies have explored this question.

Recent Advances

• Evidence from the Religious Orders Study and the Memory and Aging Project—two community-based epidemiologic studies conducted by Rush University Medical Center scientists—indicated that about one-third of individuals between the ages of 82 to 85 who did not have clinical dementia or aMCI when they died still met the neuropathologic criteria for intermediate or high likelihood of AD (Bennett et al., 2006a). In earlier tests of memory and other cognitive functions, those who met the AD neuropathologic criteria scored a little lower on tests of episodic memory (the ability to place information in long-term storage for later retrieval) than other study participants but showed no differences on other cognitive domains.
• The development of Pittsburgh Compound-B (PiB) has allowed scientists to take huge steps forward in their understanding of normal and abnormal age-related changes in the brains (Klunk et al., 2004). PiB is a radiolabeled compound that binds to beta-amyloid plaques in the brain and can be imaged in living people using positron emission tomography (PET) scans. Two recent studies conducted by researchers at Washington University School of Medicine and the Centre for PET in Victoria, Australia, showed that approximately 20 percent of 66- to 86-year-olds with normal cognition showed positive PiB binding, indicating an abundance of beta-amyloid in the brain (Mintun et al., 2006; Rowe CC et al., 2007).

These and other findings show that studies to explore further the interface between a pathological process (formation of beta-amyloid plaques) and the aging process are both feasible and necessary. Future studies will clarify the relationship between AD brain pathology and the eventual diagnosis of aMCI and AD, as well as when the diagnosis can be made with certainty.

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