Recent evidence has revealed that the physiopathological process underlying AD starts several years before the first clinical symptoms are observed ( Price and Morris, 1999 Sperling et al., 2012), and that an early diagnosis and intervention would bring demonstrable economic benefits for healthcare systems ( Barnett et al., 2014). Since AD is a major public health problem with strong psychosocial and economic impacts, early diagnosis has become an important issue. Its exact etiology remains uncertain and is thought to involve multiple factors and complex causal mechanism, with age acting as the main risk factor ( Morris and Becker, 2004). AD is currently considered the most frequent cause of dementia in developed countries. Its onset is insidious and its course progressive, increasingly impairing daily life activities. Finally, it has been established that aMCI is more likely to constitute an early form of AD than naMCI ( Petersen et al., 2009 Peraita et al., 2011).ĪD is a neurodegenerative disease characterized by the presence of cognitive and behavioral impairments. Evidence of abnormalities in neuroimaging ( Lippa and Chetelat, 2010) and the presence of the □4 allele ( Livingston et al., 2017) also increase the likelihood of conversion to AD. The likelihood of conversion and its rapidity depends on the presence of biomarkers such as abnormal levels of beta-amyloid and tau proteins in the cerebrospinal fluid (CSF) ( Petersen et al., 2010 García Ribas et al., 2014). Existing data on conversion rates to AD vary among studies, with estimates ranging between 4% and 25% ( Bozoky et al., 2000 Zaudig, 2002). The prevalence of MCI in older people ranges between 14% and 18%, with aMCI being twice as prevalent as non-amnesic (naMCI) forms ( Petersen et al., 2009). This form of MCI is known as amnestic mild cognitive impairment (aMCI). According to the National Institute on Aging-Alzheimer’s Association’s diagnostic criteria ( Albert et al., 2011), when these changes involve memory and there is positive evidence of certain biomarkers (e.g., beta-amyloid, tau, temporal atrophy, and/or frontoparietal hypometabolism), it is likely that the cognitive changes experienced by the person represent the initial symptoms of AD. It constitutes a risk factor for progression to AD dementia ( Jessen et al., 2014 Mitchell et al., 2014). Next comes mild cognitive impairment (MCI), considered an intermediate condition whereby changes in cognition exceed the normal, expected changes related to age, without affecting one person’s daily activities ( Petersen et al., 1999). Between the two ends of this continuum, subjective cognitive decline (SCD) refers to the perception of memory or other cognitive problems without impairment on standardized cognitive tests. We conclude that the FNAME test may be a valuable tool for early diagnosis but that some important questions remain to be resolved in future research.Īging involves brain and functional changes, and it is common to talk about a continuum from normal aging to Alzheimer’s disease (AD). These studies are based on the evidence that AD’s pathological process begins years before the most visible clinical manifestations. Studies looking at correlations between performance on the FNAME test and biomarkers in healthy people and studies comparing healthy controls and people with mild cognitive impairment are reviewed. The objective of this paper is to review the studies that have explored the use of the Face-Name Associative Memory Exam (FNAME) as a test for early diagnosis of AD. One current challenge for neuropsychologists is to design assessment methods capable of detecting cognitive deficits in the early or preclinical phases of Alzheimer’s disease (AD). Department of Psychology and Research Institute of Health Sciences (IUNICS), University of the Balearic Islands – Balearic Islands Health Research Institute (IdISBA), Palma de Mallorca, Spain.
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