There is evidence for an association between vascular disease and depression, and in particular between cerebrovascular disease and depression, especially that occurring later in life. Among the diverse psychiatric diseases, the one which is most widely studied concerning the relationship with the vascular system, is depression. The risk relationship between depression and vascular events is a two-way road: the presence of depression increases the cerebrovascular and cardiovascular event risk (worsening its evolution and prognosis, as well) and a patient evidencing cerebrovascular or heart disease, will also show an increase in the risk of suffering depression (Taragano et al., 2005). Depression is a common cause of disability in the elderly. It reduces quality of life and represents a serious public health problem (Beekman et al., 2001; Steffens et al., 2000). Its prevalence in late life is 2–3% for major depression and 12–15% for all depressive syndromes (Beekman et al., 1999).
Given the current controversies between the clinical and neuropathological data in Alzheimer's disease (AD), Jack et al. (2016) proposed a new biomarker based classification named as the ATN system with the goal of developing a more accurate characterization and understanding of the sequence of events that lead to cognitive impairment. Opposed to the previous concepts (Albert et al., 2011; Sperling et al., 2011), here the classification is entirely based on biomarkers (Jack et al., 2018). The seven major AD biomarkers are divided in three binary classes: "A" refers to Aβ biomarkers (amyloid PET or CSF Aβ42), "T" to tau pathology biomarker (CSF p-tau or tau PET), and "N" a quantitative or topographic biomarker of neurodegeneration (CSF t-tau, FDG-PET or structural MRI) and each biomarker is rated as positive or negative (Jack et al., 2016; 2018). The aim of this study was to describe the A/T/N research framework classification for AD in the Argentine ADNI cohort and to explore the prediction to develop dementia in a prospective two-year follow-up. A cohort of 56 individuals (23 Mild Cognitive Impairment [MCI], 12 AD and 14 controls) were studied with the ADNI-2 protocol, which has been described in detail elsewhere (Russo et al., 2014). Patients were categorized according to A/T/N and were followed longitudinally (baseline, at 12-and 24-month follow-up visits). A + /T + /N + at baseline was found in 2/14 controls (14%), 2/10 early MCI (20%), 6/13 late MCI (46%) and 11/12 mild dementia (91%); Suspected non-AD pathophysiology (SNAP, A-/T-/N +) was found in 1/14 controls (7%), 2/10 early MCI (20%), 2/13 late MCI (15%) and 1/12 mild dementia (8%); and A-/T-/N-: 8/14 (57%) of normal controls, 4/10 (40%) of e-MCI, 3/13 (23%) of l-MCI and 0/12 (0%) of mild dementia. The first two-year survival analysis was based on clinical classification among normal controls 1/14 (7%), early MCI 2/10 (20%) and late MCI 6/13 (46%). The second two-year survival analysis
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