AbstractBackgroundSentence repetition deficits have been shown to be critical in diagnosing primary progressive aphasia (PPA), particularly the logopenic variant, distinguishing its symptoms from other Alzheimer’s disease related dementias [1‐3]. These impairments were found to be associated with working memory [4].MethodIn the current preliminary study, to further investigate how sentence repetition is mediated in memory in PPA and AD, we used a spoken sentence‐span task to examine groups of 6 French‐speaking PPA (including lvPPA and non‐fluent subtypes), 6 AD patients without aphasia, and 15 healthy ageing controls. The task required individuals to repeat meaningful French sentences with increasing number of content words ranging from three to nine. Each span of content words contained two items, and when the participants failed in repeating both items in one span, the task was terminated; when one item was incorrectly repeated half a point penalty was issued.ResultsBoth the patient groups performed more poorly than healthy controls in all measures (ts>+/‐3.27). A set of mixed‐effects regression models showed that the PPA group had reduced sentence‐span (M PPA=5.08 vs. M AD=5.66; ß=0.58, SE=0.16, t=3.53, 95%CIs[0.25,0.91]), greater difficulty repeating content words (M PPA= 44.33 vs. M AD=50.00; ß=5.66, SE=2.19, t=2.57, 95%CIs[‐2.18,‐0.48]), and elevated number of substitution errors (M PPA= 6.16 vs. M AD=4.83; ß=‐1.33, SE=0.42, t=‐3.10, 95%CIs[1.32,10.01]) compared to the AD group (Figure 1). No group differences were found in repetition duration standardized by number of content words.ConclusionWe found that sentence repetition deficits in PPA have different characteristics than those in AD, submitting to earlier studies that associated PPA assessment with graphic markers [5]. We recommend clinicians to incorporate a sentence repetition task involving sentences with varying length and number of content words in their diagnostic assessment as this study suggests that working‐memory intensive sentence repetition decline appears to be a neuropsychological clinical marker distinguishing cognitive profiles of PPA from AD patients. [1]Hohlbaum, et al., Aphasiology, 2018. 32(12):1445‐1467. [2]Foxe, et al., Cortex, 2016. 83: p.39‐50. [3]Gorno‐Tempini, et al. Neurology, 2008. 71(16): p.1227‐1234. [4]Beales, et al., Brain and Language, 2019. 194: p.1‐11. [5]Gros, et al., Alzheimer’s&Dementia, 2019. P1‐285(15): p.351‐352.