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Background: In the era of disease-modifying therapies, empowering the clinical neuropsychologist's toolkit for timely identification of mild cognitive impairment (MCI) is crucial. Objective: Here we examine the clinimetric properties of the Montreal Cognitive Assessment (MoCA) for the early diagnosis of MCI due to Alzheimer's disease (MCI-AD). Methods: Data from 48 patients with MCI-AD and 47 healthy controls were retrospectively analyzed. Raw MoCA scores were corrected according to the conventional Nasreddine's 1-point correction and demographic adjustments derived from three normative studies. Optimal cutoffs were determined while previously established cutoffs were diagnostically reevaluated. Results: The original Nasreddine's cutoff of 26 and normative cutoffs (non-parametric outer tolerance limit on the 5th percentile of demographically-adjusted score distributions) were overly imbalanced in terms of Sensitivity (Se) and Specificity (Sp). The optimal cutoff for Nasreddine's adjustment showed adequate clinimetric properties (≤23.50, Se = 0.75, Sp = 0.70). However, the optimal cutoff for Santangelo's adjustment (≤22.85, Se = 0.65, Sp = 0.87) proved to be the most effective for both screening and diagnostic purposes according to Larner's metrics. The results of post-probability analyses revealed that an individual testing positive using Santangelo's adjustment combined with a cutoff of 22.85 would have 84% post-test probability of receiving a diagnosis of MCI-AD (LR+ = 5.06). Conclusions: We found a common (mal)practice of bypassing the applicability of normative cutoffs in diagnosis-oriented clinical practice. In this study, we identified optimal cutoffs for MoCA to be allocated in secondary care settings for supporting MCI-AD diagnosis. Methodological and psychometric issues are discussed. [ABSTRACT FROM AUTHOR]

Many studies have attempted to determine whether Alzheimer's disease (AD) in-vivo biomarkers can predict neuropsychological performance since pathophysiological changes precede cognitive changes by several years. Nonetheless, neuropsychological measures can also detect cognitive deterioration in cognitively normal individuals with AD-positive biomarkers. Recent studies have investigated whether cognitive measures can be used as a proxy for biomarkers. This is a crucial issue since biomarker analysis is expensive, invasive, and not yet widespread in clinical practice. However, these studies have so far considered only one or two classes of AD biomarkers. Here, we aim at preliminarily evaluating whether and which neuropsychological measures can discriminate individuals that have been classified according to the full scheme of biomarkers known as ATN system. This scheme groups biomarkers as a function of the three main AD-related pathologic processes they measure (i.e., β-amyloidosis, tauopathy, and neurodegeneration) to provide an unbiased and descriptive definition of the Alzheimer's continuum. Biomarkers and neuropsychological data from 78 patients (70.01 ± 9.15 years; 38 females) with suspected cognitive decline were extracted from a medical database. Participants' biomarker profiles were classified into the following ATN categories: normal AD biomarkers; Alzheimer's continuum; non-AD pathologic change. Data were analyzed using a Bayesian approach, to guarantee reliable result interpretation of data stemming from small samples. The discrimination ability of each neuropsychological measure varied depending on the pairs of ATN categories compared. The best-discriminating predictor in the Alzheimer's continuum vs. normal biomarkers comparison was the figure naming ability. In contrast, in the Alzheimer's continuum vs. non-AD pathologic change comparison the best predictor was the wordlist forgetting rate. Although the study was exploratory in nature, the proposed methodological approach may have the potential to identify the best neuropsychological measures for estimating AD neuropathological changes, leading to a more biologically informed use of neuropsychological assessment. [ABSTRACT FROM AUTHOR]

The peculiar pattern of linguistic and cognitive deficits in early Alzheimer’s disease (DAT), whereby memory limitations and failure in semantics prevail over deficits in syntax, makes an interesting contrast with linguistic deficits in classic aphasia categories. The present study compared errors in picture naming of different types of Italian compounds, both in aphasia and in DAT. As in previous studies, in aphasia the knowledge of the compound status seems to be retained vis-à-vis the inability to retrieve the phonological form. This effect is much less evident in DAT. The target compound structure in errors is also preserved in aphasia, while DAT participants seem to compensate for their retrieval failure by overwhelmingly using the most productive structures. Unlike in aphasia, in DAT the retrieval of the second component is more difficult than the retrieval of the first component, probably as an effect of processing overload. [ABSTRACT FROM AUTHOR]