The paper:
K.E. Pike et al., “Beta-amyloid imaging and memory in non-demented individuals: evidence for preclinical Alzheimer’s disease,” Brain, 130:2837–44, 2007. (Cited in 83 papers)

The finding:
One of the hallmarks of Alzheimer’s disease (AD) is the build-up of the abnormal peptide ß-amyloid in the brain, although it’s not clear just how amyloid is involved in the disease. To determine whether ß-amyloid levels correlate with memory loss in general, Christopher Rowe at the Austin Hospital in Australia and his colleagues compared the amount of ß-amyloid in normal adults and patients with varying degrees of memory loss. They found that patients with even early signs of memory impairment had higher levels of amyloid than normal adults.

The caveat:
Among patients with established Alzheimer’s disease, those with more memory loss did not have higher levels of amyloid, a finding supported by earlier studies.

The implications:
The paper “suggests that the amyloid is playing a very early role [in Alzheimer’s],” says lead author Christopher Rowe. Furthermore, the accumulation of amyloid appears to trigger changes in the brain that ultimately result in the cognitive decline, says William Jagust, a neuroscientist at the University of California, Berkeley. Consequently, the time to target amyloid plaques would be the early stages of the disease, perhaps before it is even diagnosed by cognitive tests.

The future:
Rowe and his colleagues have initiated a long-term prospective trial to track amyloid and other markers in more than 1,000 people, healthy and with memory decline, as they age.

Percentage of participants with ß-amyloid plaques:

Alzheimer’s disease: 97%

Mild cognitive impairment: 61%

Healthy aging cases: 22%

It would be nice to be able to link to the evaluation in F1000.

At one point in the article, the language is appropriate -- CORRELATION. The accumulation of amyloid plaque has been shown to CORRELATE with memory loss. The accumulation of plaque seems to occur early in the memory-loss process. All that is supported by the data.

But to infer from the data that the accumulation of plaque is the causative factor is totally inappropriate !!! It's a hypothesis that may (or may not, at the present time) be testable, but it's certainly not a valid inference from the data. Of at least equal plausibility is the hypothesis that some physiological process, enzymatic or otherwise, that leads either directly or indirectly to the accumulation of plaque, is also responsible either directly or indirectly for the memory loss observed. This too may or may not be easily testable at the present time.

C'mon folks -- are we scientists or not?

More detail on their study would allow evaluation and knowledge transfer!