The YKL-40 levels of MCI-AD and AD dementia patients did not differ (Fig. 1).
Diagnostic standards for all-cause dementia are provided, and 10 categories of dementia of the AD type - including probable AD dementia, possible AD dementia, probable or possible AD dementia with evidence of the AD pathophysiological process, and pathophysiologically proved AD dementia - are established [ 18].
Based on this evidence the 11.7 kDa protein species was isolated from a pool of CSF from AD dementia cases (CDR 2; moderate AD dementia) and sequence identified as S100A7 based on MS criteria.
This diagnosis would be analogous to the NIA-AA diagnosis of probable AD dementia with evidence of the AD pathophysiological process [ 60].
The mean MSLT initial sleep latency was shorter for DLB than AD dementia (DLB =6.4 ± 5 minutes vs AD dementia =11.3 ± 5 minutes, F =12.6, P <0.01).
The person with the AD dementia phenotype and no biomarkers would receive a diagnosis of probable AD.
CSF YKL-40 levels were significantly elevated in patients with AD dementia as compared with those with MCI-o or non-AD dementia (p < 0.05).
We hypothesized that CSF and PET would have equal diagnostic performance, both when testing healthy controls versus AD dementia patients, and when testing stable MCI patients versus MCI patients who later progressed to AD dementia.
Studies on markers of inflammation in subjects with mild cognitive impairment or AD dementia provided inconsistent results.
It is estimated that the total number of the elderly Americans with Alzheimer disease (AD) dementia is projected to be approximately 14 million in 20503.
Estimates have suggested that delaying the onset of AD dementia by just five years would reduce the economic burden by 36% by 20505.
