By age 40, most if not all DS patients have extensive amyloid plaque pathology and degeneration of basal forebrain cholinergic neurons, both characteristic features of AD, and most of these individuals develop AD dementia by the fifth and sixth decades of life [9].
They acknowledge that 'the definitive studies to determine whether the majority of asymptomatic individuals with evidence of AD-P are indeed destined to develop AD dementia... will likely take more than a decade to fully accomplish' ([ 3], p. 11).
Additionally, two subsamples of this normative sample were considered to examine potential differences in the number of low scores (see " Analyses" section) already at this stage of normalcy between participants who later developed AD dementia (NC AD) and participants who remained cognitively healthy (NC NC).
Notably, a meta-analysis of 13 studies of populations in the US, Europe, and Asia did show that women were at a significantly greater risk of developing AD, but not other dementias.
In a pilot study, high sphingomyelin levels predicted an increased risk of developing AD while plasma levels of glucosylceramide predicted Lewy-body dementia disease severity.
Although the risk of developing AD and PD increases with age, neither of these diseases nor the symptoms of dementia are part of normal aging.
Two studies used incident cases of dementia from cohort studies and exposure to GA was determined through interviews of individuals prior to them developing AD.
Family history of dementia was ascertained, excluding all the subjects with even one relative who developed AD or other dementias.
The Non-AD (The test set samples include Other Dementia (OD) samples, which have not developed AD but are still demented controls) samples are marked in green, and the samples labelled AD are marked in blue.
