Clinically normal participants (CN) (n = 264) were included if they had a Clinical Dementia Rating (CDR) score of 0, DCTclock, and standard neuropsychological tests including the Primary Alzheimer Cognitive Composite (PACC). In total, 300 participants were recruited from the Harvard Aging Brain Study (HABS) and separate imaging protocols from the MGH PET laboratory. This cross-sectional study was conducted at Massachusetts General Hospital (MGH) using protocols and informed consent procedures approved by the Partners Human Research Committee. ![]() We also hypothesized that digital clock performance scores would have a greater association with PET amyloid and tau deposition in CN older adults than traditional paper and pencil cognitive tests. We used the digital clock-drawing test (DCTclock), obtained from Digital Cognition Technologies, to explore whether this digitized measurement approach would be clinically useful for discriminating cognitively normal (CN) from diagnostic groups. 5, 6 This simple test taps into a wide range of cognitive domains including executive functioning, visuospatial abilities, and semantic memory and has shown high sensitivity for discriminating cognitive decline from normal performance in the clinical setting. 4 We explored whether a digital cognitive test, designed to elicit multiple performance features not available in traditional cognitive formats, could be useful for this purpose.įor nearly a century, clock-drawing tests have been used to assess the mental status of patients and is one of the most widely used screening tests for cognitive impairment in AD. ![]() ![]() 2, 3 Furthermore, traditional cognitive screening tests were not designed to correlate with these early biomarker abnormalities. Amyloid and tau PET biomarkers of AD pathology can detect evidence of preclinical AD in asymptomatic individuals, but they are costly and inaccessible in the clinical setting. 1 Identifying individuals at risk for AD will be critical as prevention trials or potential treatments become available. Alzheimer disease (AD) is a continuum, with the pathophysiologic brain changes of β-amyloid (Aβ) plaques, neurofibrillary tau tangles, and subsequent neurodegeneration occurring 15–20 years before the clinical stage of AD dementia.
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