**1. Introduction**

In recent decades, population aging has led to an increase in the number of people affected by cognitive impairment, this becoming a major problem both clinically and socially, especially in Western countries [1,2]. In this sense, while in 2016 there were 47.5 million people diagnosed with dementia, in 2050 it is expected to affect more than 135.5 million individuals [3], with Alzheimer's disease (AD) and vascular dementia (VD) the most common form of dementia [2,4,5].

However, the big problem with these diseases is not their frequency nor their growth forecasting, but their late diagnosis. The lack of differentiation between normal processes of cognitive impairment and disease states, coupled with the characteristic features of dementia—with an appearance that tends to be insidious and a development that tends to extend over time [6]—makes the first symptoms of dementia and AD easily go unnoticed [7,8]. Therefore, patients suffering from these diseases are diagnosed too late, when neurological symptoms are actually noticeable and the disease is already in very advanced stages [9]. In fact, previous studies point to how AD probably begins decades before the first symptoms appear [10]. As a result, the identification of risk/prodromal factors becomes essential to prevent the disease and, especially, to prevent late detection/diagnosis of the disease.

The association between this disease and many risk factors has been described. Some of them, such as dyslipidemia, hypertension, or tobacco use, have clear pathophysiological mechanisms because of their vascular component [11,12]. Nevertheless, this would not be the only association between dyslipidemia and AD since recent animal studies have shown how hypercholesterolemia may favor β-amyloid deposits characteristic of AD and therefore be related to neuroinflammation and loss of neuronal function [13]. However, despite being considered a risk factor for the development of AD, the pharmacological approach to this cardiovascular risk factor in older people would not prevent the onset of AD nor slow the course of neurodegenerative disease. This leads us to question the link described above between dyslipidemia and AD [14,15].

Other risk factors, such as type 2 diabetes mellitus (T2DM), seem to have a bidirectional relationship with AD, because it involves modifications in vascular function and structure, glucose metabolism, and insulin signaling, thus contributing to neurodegeneration [16–18]. In fact, both dementia and T2DM share symptoms, such as inflammation and altered insulin signaling mechanisms [19]. However, the relationship between the metabolism of tau and β-amyloid proteins has not yet been elucidated [20], so while some authors focus their research on understanding the link between this accumulation and the existence of other factors, such as amylin (protein co-secreted with insulin), others analyze whether the accumulation may be part of the diabetic phenotype [21,22].

Finally, others, such as anxiety and depression seem to be related to the appearance of dementia. However, while recent studies have described anxiety as a risk factor of AD, increasing the risk of this neurodegenerative disease by up to 50% [23], the exact link between depression and dementia is unknown and controversial, to the point of not knowing if depression is associated with a future development of AD and if it could be considered a risk factor for AD, or if, on the contrary, depression is a consequence of AD [24–26]. It appears that depressive symptoms in older adults with cognitive impairment may be related to the distinctive amyloid and tau signs of AD [27,28], thus establishing an association between depressive symptoms and cognitive impairment in older adults [29].

In this sense, the prevailing depressive symptoms among older adults could be considered modifiers of cognitive performance, but they could also be clinical indicators or early clinical signs and symptoms of AD [30,31], which would justify a comprehensive management of neuropsychological functioning in older people diagnosed with depression, regardless of the age of onset and the disease pattern (self-limiting, incident or persistent).

In this way, prevention of the onset of dementia would involve, first, assessing and adequately diagnosing this mental disorder and, second, addressing it with appropriate pharmacological and non-pharmacological treatment [32,33].

In this context, the aim of this study was to elucidate the association between depression and dementia/AD and to identify possible relationships between these diseases and different sociodemographic and clinical features.
