Landau et al. present very intriguing work. Their cross-sectional results suggest that cognitive activity before the age of 40 years may influence fibrillar amyloid plaque deposition. I was frankly surprised to see how high the Spearman correlation was (r = -.37) between lifetime cognitive activity and amyloid uptake, and would be interested to know the magnitude of this correlation when confined to early and midlife cognitive activity. The finding that both past cognitive activity and educational level (p = .052) were associated with PIB uptake is logically congruent and strengthens confidence in these results.
I look forward to seeing the results of longitudinal studies along these lines. I imagine that Landau et al. will follow these participants forward in time to see whether those with higher PIB uptake are, in fact, faster to develop AD (which is likely based on other research), and to determine whether, in line with the cognitive and brain reserve hypotheses (e.g., Stern, 2006; Mortimer, 1997), greater early-life cognitive activity is also associated with a slower time to development of AD after controlling for amount of amyloid uptake level. Our Adult Child Study, led by John Morris, may also help to inform these questions. We are assessing AD biomarkers along with cognitive and physical activity in middle-aged adults, and are following these adults forward in time to examine predictors of incident dementia. If the results of Landau et al. can be confirmed in longitudinal studies, this would strengthen the increasingly hard-to-ignore argument that lifestyle factors, and individual differences, are important influences in the development of symptomatic AD.
References:
Stern Y.
Cognitive reserve and Alzheimer disease.
Alzheimer Dis Assoc Disord. 2006 Apr-Jun;20(2):112-7.
PubMed.
Mortimer JA.
Brain reserve and the clinical expression of Alzheimer's disease.
Geriatrics. 1997 Sep;52 Suppl 2:S50-3.
PubMed.
Comments
Landau et al. present very intriguing work. Their cross-sectional results suggest that cognitive activity before the age of 40 years may influence fibrillar amyloid plaque deposition. I was frankly surprised to see how high the Spearman correlation was (r = -.37) between lifetime cognitive activity and amyloid uptake, and would be interested to know the magnitude of this correlation when confined to early and midlife cognitive activity. The finding that both past cognitive activity and educational level (p = .052) were associated with PIB uptake is logically congruent and strengthens confidence in these results.
I look forward to seeing the results of longitudinal studies along these lines. I imagine that Landau et al. will follow these participants forward in time to see whether those with higher PIB uptake are, in fact, faster to develop AD (which is likely based on other research), and to determine whether, in line with the cognitive and brain reserve hypotheses (e.g., Stern, 2006; Mortimer, 1997), greater early-life cognitive activity is also associated with a slower time to development of AD after controlling for amount of amyloid uptake level. Our Adult Child Study, led by John Morris, may also help to inform these questions. We are assessing AD biomarkers along with cognitive and physical activity in middle-aged adults, and are following these adults forward in time to examine predictors of incident dementia. If the results of Landau et al. can be confirmed in longitudinal studies, this would strengthen the increasingly hard-to-ignore argument that lifestyle factors, and individual differences, are important influences in the development of symptomatic AD.
References:
Stern Y. Cognitive reserve and Alzheimer disease. Alzheimer Dis Assoc Disord. 2006 Apr-Jun;20(2):112-7. PubMed.
Mortimer JA. Brain reserve and the clinical expression of Alzheimer's disease. Geriatrics. 1997 Sep;52 Suppl 2:S50-3. PubMed.
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