Objectives To assess plasma phosphorylated tau181 (p‐tau181) levels in Alzheimer's disease (AD), cognitively impaired non‐AD participants (CI non‐AD) and Control participants in the Alzheimer's Disease Neuroimaging Initiative (ADNI) dataset that could potentially act as reference data for clinic diagnoses of AD. Methods Data from 1558 participants (649 AD participants, 445 CI non‐AD participants and 464 controls) were examined, comparing p‐tau181 levels between Controls, AD and other dementias, stratified by age. Results There were significant differences in plasma p‐tau181 values between Controls and those with AD at all ages up to 85 years. There were also significant differences between AD and CI non‐AD participants up to the age of 85 years. Conclusions Plasma P‐tau181 may be a useful tool in the diagnosis of AD in those clinical settings where biomarkers have traditionally been less used. P‐tau181 may be less useful as an aid to diagnosis in the very oldest‐old. Further work is needed to establish the feasibility and utility of this biomarker within dementia diagnosis services not led by Neurologists, such as UK National Health Service Memory Services.
Background In Alzheimer’s disease (AD), temporal lobe pathology begins years before onset of clinical symptoms1. Early detection of temporal lobe dysfunction would be valuable for trials. Accelerated long‐term forgetting (ALF) – failure to recall learnt material when the interval of testing is extended to days as opposed to the traditional interval of minutes – has been shown to be a sensitive measure of early cognitive change in AD. However, it is not clear if ALF can predict future progression. Here we investigate the prognostic utility of ALF by assessing whether baseline performance is associated with subsequent cognitive and clinical decline. Method Thirty‐five at‐risk participants were recruited from UCL’s Longitudinal Cohort Study of Familial Alzheimer’s Disease (FAD). At baseline ALF was assessed by comparing recall performance at 7 days to performance after a 30‐minute interval. Visual (figure) and verbal (list and story) measures were used. Annual follow‐up visits included a detailed neuropsychological battery, mini‐mental state examination, Clinical Dementia Rating scale (CDR), measures of anxiety and depression and subjective memory decline. We tested for an association between baseline performance in ALF and rates of change in cognitive and clinical measures. Results At baseline, mean time to estimated symptom onset (based on parental age at onset) for mutation carriers was 7.2 years (SD 4.5 years). Four mutation carriers became symptomatic (CDR>0); baseline performance in these cases was in the 5th‐23rd percentiles for verbal measures of ALF. We will present the value of accelerated long‐term forgetting in predicting cognitive decline in this cohort. Conclusion ALF is a feature of presymptomatic AD with potential utility in stratification and prognostication. References: 1. Bateman, R.J. et al. N. Engl. J. Med. 367, 795–804 (2012). 2. O’Connor, A. et al. Alzheimer’s Res. Ther. 12, 1–9 (2020).
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