Longitudinal results in the CN population and MCI and sporadic AD

Longitudinal results in the CN population and MCI and sporadic AD cases Different measures of plasma A?? have been associated with progression to dementia (Table ?(Table4):4): high baseline A??1-42 [30,57], low baseline A??1-42/A??1-40 [58,59], low baseline A??1-40 read more or A??1-42 [60], high baseline A??1-40 [29], high A??1-40 or low A??1-42/A??1-40 [61] and low A??1-40 in older subjects [62]. Finally, other studies found no associations of plasma A?? levels with progression to dementia [10,13,63]. A study including information on vascular risk factors in midlife and a long follow-up period after baseline plasma sampling found an increased risk of dementia in subjects with low A??1-40 and A??1-42 at baseline and there was an interaction between plasma A?? levels and diastolic blood pressure that indicated a higher incidence of dementia in subjects with higher diastolic blood pressure and low plasma A?? levels [60].

One study that compared A?? plasma levels in CN and MCI subjects who remained cognitively stable or progressed to AD found no differences in these two different cohorts [13], but, as noted above, there were significant differences based on the CSF-defined groups. Table 4 Longitudinal studies in populations including sporadic Alzheimer’s disease patients Other studies measuring plasma A?? levels included correlations of these values with cognitive measures instead of using a diagnosis as outcome. One study included 481 subjects with a long follow-up and repeated measurements, and it used repeated brief telephone interviews for determining the study outcome, and the authors reported greater cognitive decline in subjects with a low A??1-42/A??1-40 at baseline [64].

However, interassay CV was over 30% (repeated subject measurements were included in the same assay with CV <10%). A larger study of 997 CN subjects followed for 9 years also found a faster cognitive decline in subjects with a lower A??1-42/A??1-40 at baseline [65]. Cosentino et al. [66] followed 880 subjects for 4.5 years who were CN at baseline or had cognitive impairment that was not severe enough for a dementia diagnosis. In this study, subjects with higher baseline A??1-40 and A??1-42 and stable or decreasing A??1-42 levels during follow-up had a faster rate of decline, whereas A??1-42/A??1-40 showed no such association. On the other hand, in another study by Locascio et al.

[67], the rate of cognitive decline in 122 AD patients was Entinostat determined in subjects followed for 4.2 years, and these authors described a faster decline in subjects with lower plasma A??1-40 and A??1-42 at baseline. Two studies found an interaction between cognitive reserve ref 1 and A?? plasma levels, indicating that subjects with lower cognitive reserve showed a greater decline associated with A?? levels [10,65].

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