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INTRODUCTION: With emergence of disease‐modifying therapies, efficient diagnostic pathways are critically needed to identify treatment candidates, evaluate disease severity, and support prognosis. A combination of plasma biomarkers and brief digital cognitive assessments could provide a scalable alternative to current diagnostic work‐up. METHODS: We examined the accuracy of plasma biomarkers and a 10‐minute supervised tablet‐based cognitive assessment (Tablet‐based Cognitive Assessment Tool Brain Health Assessment [TabCAT‐BHA]) in predicting amyloid β positive (Aβ+) status on positron emission tomography (PET), concurrent disease severity, and functional decline in 309 older adults with subjective cognitive impairment (n = 49), mild cognitive impairment (n = 159), and dementia (n = 101). RESULTS: Combination of plasma pTau181, Aβ42/40, neurofilament light (NfL), and TabCAT‐BHA was optimal for predicting Aβ‐PET positivity (AUC = 0.962). Whereas NfL and TabCAT‐BHA optimally predicted concurrent disease severity, combining these with pTau181 and glial fibrillary acidic protein was most accurate in predicting functional decline. DISCUSSION: Combinations of plasma and digital cognitive markers show promise for scalable diagnosis and prognosis of ADRD. Highlights: The need for cost‐efficient diagnostic and prognostic markers of AD is urgent.Plasma and digital cognitive markers provide complementary diagnostic contributions.Combination of these markers holds promise for scalable diagnosis and prognosis.Future validation in community cohorts is needed to inform clinical implementation. [ABSTRACT FROM AUTHOR]

The article discusses research which examined gaps in primary care diagnosis of cognitive impairment via a telephone-based nurse consultation and proposed a care model that could help address unmet needs of patients and care partners. Study findings revealed concerns about memory loss, word finding, or other cognitive changes, as well as neuropsychiatric symptoms, problems with sleep and pain and activities of daily living difficulties. Gaps in advanced care planning were identified.

As they form, synapses go through various stages of maturation and refinement. These steps are linked to significant changes in synaptic function, potentially resulting in emergence and maturation of behavioral outputs. Synaptotagmins are calcium‐sensing proteins of the synaptic vesicle exocytosis machinery, and changes in Synaptotagmin proteins at synapses have significant effects on vesicle release and synaptic function. Here, we examined the distribution of the synaptic vesicle protein Synaptotagmin 2a (Syt2a) during development of the zebrafish nervous system. Syt2a is widely distributed throughout the midbrain and hindbrain early during larval development but very weakly expressed in the forebrain. Later in development, Syt2a expression levels in the forebrain increase, particularly in regions associated with social behavior, and most intriguingly, around the time social behavior becomes apparent. We provide evidence that Syt2a localizes to synapses onto neurons implicated in social behavior in the ventral forebrain and show that Syt2a is colocalized with tyrosine hydroxylase, a biosynthetic enzyme in the dopamine pathway. Our results suggest a developmentally important role for Syt2a in maturing synapses in the forebrain, coinciding with the emergence of social behavior. [ABSTRACT FROM AUTHOR]