## 1 Introduction  
Addressing dementia is a crucial public health issue, as well as a major health and social problem. It has now become the silent epidemic of the 21 st century and is one of the greatest challenges to the sustainability of health and social care systems [1]. The current prevalence of dementia worldwide is estimated at 50 million people over 65 years of age and it is expected that these figures will triple, reaching about 150 million by 2050 [2]. This mainly as a consequence of the progressive increase in aging given the greater life expectancy of the population worldwide, as well as the increase in other risk factors such as metabolic, environmental and personal factors [3].  
Among the dementias, Alzheimer's disease (AD) stands out. AD is a neurodegenerative disease specifically affecting certain brain areas such as the neocortex or the hippocampus [4]. AD is characterised by both microscopic and macroscopic neuropathological changes. At the microscopic level, accumulation of beta-amyloid (AB) peptide and hyperphosphorylated Tau (\(\tau\)) protein results in extracellular senile plaques and intracellular neurofibrillary tangles, as well as early and steady synaptic loss [5]. At the macroscopic level, significant brain atrophy is observed due to loss of neural and synaptic tissue, correlated with disease progression and cognitive decline [4]. Also, neuroinflammation, oxidative stress and damage to cholinergic neurons contribute to the pathological process of AD [6].  
The risk factors for AD are the result of a complex interaction between an individual's genetic predisposition and exposure to modifiable risk factors, called environmental factors [7]. Both types, genetic and environmental factors, could serve as prognostic biomarkers and early diagnostic tools for AD [8]. On the one hand, genetic factors are non-modifiable risk factors inherent to the person, such as the \(\epsilon\)4 allele polymorphism of the Apo E gene, as the most prevalent [9]. Other non-modifiable risk factors are gender, race or ethnicity and family history [10]. On the other hand, modifiable risk factors are influenced by a person's decisions and actions, which means that they can be acted upon [10; 11]. In fact, modifiable risk factors contribute substantially to the development of AD [11]. However, the actions and management of these factors would significantly reduce the risk of suffering from AD [10]. In this sense, the study conducted by [PERSON] et al. [12] estimated that if modifiable risk factors could be reduced by 10% to 25%, 3 million cases of AD could be prevented worldwide. The modifiable risk factors most associated with AD are low educational level [12], diet [13], sedentary lifestyle [14] and cardiovascular risk factors [15]. In this way, [PERSON] et al. [15] have studied ApoE, cholesterol metabolism and diabetes mellitus (DM), suggesting a convergence of these factors with cardiovascular disease and AD [15]. In addition, metabolic disorders such high blood pressure (HBP), hypercholesterolemia or obesity increase the predisposition to AD (23). Previous findings [16; 17] would support the idea that there could be a link between AD and cardiovascular disease. AD and cardiovascular disease share common risk factors and similarities in the triggering molecular mechanisms, shown in Figure 1. In addition, it should be noted that the \(\epsilon\)4 Apo E gene polymorphism affects the cardiovascular and the nervous systems [9].  
Therefore, our study aims to evaluate the possible association between key cardiovascular factors and the development of AD. This observatio  
Figure 1: Pathophysiological connections between Alzheimer’s disease and cardiometabolic comorbidities.  
be carried out in \"probable AD patients\" (pAD), without the visualization of plaques and tangles within the brain by autopsy or neuroimaging, in a region of Spain, Castilla y Leon. This study would allow personalizing future interventions on modifiable risk factors in day centres for pAD.