Introduction

In a keynote lecture at the Human Amyloid Imaging conference, held 12-13 January 2012 in Miami, Florida, Claudia Kawas argued that the oldest old should receive more attention. Kawas leads the world’s largest study of people 90 and older.

The very old are at high risk for diseases such as Alzheimer’s and stroke, yet science knows little about them. Their number is set to quadruple by 2050, average life expectancy in the U.S. has jumped by 27 years in the past century, and aging is the biggest risk factor for these expensive diseases. But because diagnostic criteria for AD include people only through their eighties, older folks are excluded from ADNI and other research studies.

If a toddler’s brain differs from that of a teenager, the 95-year-old brain likewise is not simply a worse version of the 30-year-old brain. It, too, is different, says Kawas, and it’s time to study it. Her research dates back to the 1980s, when 14,000 people in a California retirement community filled out mail surveys over the next 20 years. In 2003, most of the participants who had reached their nineties enrolled in the 90+ Study, and since then more people from other communities have swelled its ranks to 1,600 participants in 36 states. The survey phase of the research showed that, among the factors purported in the literature to affect longevity, most had no effect, but exercise and leisure activities did. Later, Kawas showed that the incidence of AD inexorably doubles with age in the nineties just as it does in the seventies and eighties, reaching a whopping 40 percent by age 100. What caused dementia in those who had survived that long? Among the proposed dementia risk factors, none appears to be important in this cohort. At autopsy, about half of those with dementia at death met NIA/Reagan pathologic criteria for AD, as did half of those without. The former declined no faster in the years before they died than the latter. On the other hand, total amyloid area of the brain did correlate with decline, and, to Kawas’ surprise, participants who were positive on an amyloid PET scan dropped off precipitously in their cognition soon after, unlike those whose scans were negative.

Kawas recorded her talk on Alzforum’s Webinar platform to share her insight with a wider audience. Play the recording, and comment below.

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Comments on this content

  1. I enjoyed the airbag analogy, though I think it's hard to say that Aβ has a "protective" role. Certainly, people can live with plaques and remain cognitively intact. I think we need to clearly understand the function of full-length APP. Presumably it serves the cell in some capacity other than as a substrate for Aβ production! Once we understand what this role is, we might be better situated to see what aberration in this function results in APP's amyloidogenic processing.

References

Other Citations

  1. Listen to the keynote lecture.

Further Reading

Papers

  1. . Oligodendrocyte precursor cells reprogrammed to become multipotential CNS stem cells. Science. 2000 Sep 8;289(5485):1754-7. PubMed.
  2. . Neocortical and hippocampal amyloid-β and tau measures associate with dementia in the oldest-old. Brain. 2011 Dec;134(Pt 12):3708-15. PubMed.
  3. . Studies in the Oldest Old: The 90+ Study. Human Amyloid Imaging Abstract. 2012 Jan 1;
  4. . Improving patient-centered care for people with dementia in medical encounters: an educational intervention for old age psychiatrists. Int Psychogeriatr. 2010 Feb;22(1):129-38. PubMed.