Abstract :
[en] Objective : Late-life depression (LLD), mild cognitive impairment (MCI) and early stage of Alzheimer's disease (AD) can share a similar pattern of cognitive impairment(Gasser et al., 2018; Leyhe et al., 2017; Potter et al., 2013; Rotomskis et al., 2015), even if they don't share the same functional causes(Goodwin, 2016; Kohler et al., 2010; Sami et al., 2018). However, this overlap of cognitive profile, which is challenging for differential diagnosis between these pathologies, is not expected to involve the impairment of semantic memory (SM): indeed, it has been demonstrated that the SM decline in AD expresses itself through a hierarchical and ordered pattern specifically related to the physiopathology of the disease(Laisney et al., 2011; Perri et al., 2019; Simoes Loureiro & Lefebvre, 2016; Venneri et al., 2008). On the contrary, the alteration of SM in LLD, whether it is spared or not, is actually left with many blind spots(Elderkin-Thompson et al., 2011; Morimoto et al., 2011; Rajtar-Zembaty et al., 2017; Zahodne et al., 2014). One of them is the time-lagged and/or causal relationships between LLD and AD(Elderkin-Thompson et al., 2011; Morimoto et al., 2011; Rajtar-Zembaty et al., 2017; Zahodne et al., 2014). Three key questions were addressed in this review. First, does the presence of depressive symptoms predict the incidence of AD or the conversion from MCI to AD? Second, in the general ageing population, is there an association between the presence of depressive symptoms and the performances in semantic tasks? Third, is semantic memory differently affected by LLD or MCI and AD?
Method : Key questions were included in a systematic review of the scientific literature of the last 10 years. Key words were selected to cover the topics of the relationship between LLD and AD or MCI, and how the diseases involve different results on SM tests. Using PRISMA's guidelines for systematic reviews(Liberati et al., 2009), we finally selected 41 research. According to the topics, quantitative data, such as scores in neuropsychological assessments, were extracted and compared. Because of the important variety of depression criteria, data about the kind of diagnostic of LLD were also systematically reviewed and included in the general analysis.
Results : LLD is indeed associated to a development towards AD but only in the presence of some characteristics of depressive state like high severity, first onset late in life and specific depressive symptoms. These data also show that SM is significantly more impaired by AD than by LLD, but that the differences are less sharped between LLD and MCI.
Conclusion : This review supports the idea that authentical LLD (not prodromal to a neurogenerative process) expresses itself through a cognitive pattern from which semantic impairment is excluded. For several studies included in this review, when a lack of differences was pointed out for semantic results between the pathologies, the tests involved were characterized by a strong executive dimension. Therefore, it raises the issue of the executive functions involved in the retrieval and selection processes rather than the question of a specific impairment of SM resources. Furthermore, data collected in this review support the hypothesis that a diagnostical pattern including LLD and authentical semantical impairment will be predictive of development towards AD. Finally, this review led to two recommendations for future investigations designed to distinguish LLD from AD (or MCI): the strict definition of what is meant by LLD (with control of diagnostical criteria, severity, onset time, subdimensions) and the use of tests measuring the differences between SM integrity and the executive functions involved in peripherical processes of semantic retrieval.
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