**1. Introduction**

The impact of brain aging on cognition is far from uniform, ranging from perfect fitness to cognitive impairment. The prevalence of dementia is estimated to increase from 57.4 million in 2019 to 152.8 million in 2050 [1], thus representing a major public health problem. Still, evidence shows that more than one-third of all cases of dementia could be prevented or modified by changes in lifestyle, correction of risk factors, and specific therapeutic interventions [2–5]. In fact, despite the absence of pharmacological treatment for degenerative diseases, such as Alzheimer's disease (AD), it is known that vascular risk factors increase the likelihood of cognitive decline. Simple measures, the control of hypertension, for instance, may revert cognitive impairment and reduce conversion to dementia [6]. Likewise, healthy lifestyle patterns, physical exercise, and intellectual and social enrichment may improve performance and change the biomarker trajectories of individuals classified as cognitively impaired [7–9].

Promoting the presence of protective factors throughout life may help to cope with the negative consequences of pathology through resilience or resistance mechanisms. The term "resistance" refers to the notion of avoiding pathology (i.e., being free from significant AD pathology) in the sense that it is inferred from an observed absence or lower level of dementia-associated brain injury, relative to an expected greater frequency or severity based on age, genetic factors, or other individual characteristics. On the other hand, "resilience" is mostly used in the sense of coping with pathology (i.e., remaining cognitively intact despite significant AD pathology) and is inferred from the observation of a higher than expected cognitive functioning related to the level of brain injury [10, 11]. While the first is linked to an absence or delay of brain changes ("brain maintenance"), the latter is closely associated with the concept of the reserve, which can be measured or inferred either as brain structural and/or physiological premorbid capacity [11, 12].

The construct of reserve firstly emerged to describe patients with extensive destruction of nervous tissue following brain damage but not the expected level of functional changes [13]. It was then proposed that larger brains, with greater weight and a larger number of neurons, could have protective effects on the cognitive decline due to a higher "brain reserve" capacity [14]. Years later, Stern [15] defined the concept of Cognitive Reserve (CR) as the brain's ability to optimize and maximize performance through the differential recruitment of brain networks or the use of alternative cognitive strategies to cope with brain dysfunction. Stern's proposal claims that the mechanisms underlying CR are active processes by which the brain tries to compensate for the neural loss. These processes can be influenced by the interaction between innate factors (e.g., in utero or genetically determined) and, mainly, lifelong experience (e.g., intelligence, education, occupation, physical exercise, leisure activities, or social involvement). In contrast, the passive models propose that response to neural damage is related to brain size or the number of synapses (brain reserve), which can affect the threshold for clinical expression [16]. Brain reserve and CR are not mutually exclusive in the sense that brain reserve does not protect against the accumulation of pathology, but it does protect against its negative effects [17]. Instead, they influence each other—life experiences and the involvement in stimulating cognitive activities can modify brain anatomy (i.e., neurogenesis, angiogenesis, and resistance to apoptosis) and positively regulate compounds that promote neural plasticity [18].

The concept of CR has progressively evolved in such a way that it is now central in the literature on normal and pathological aging, notwithstanding the theoretical pitfalls and methodological controversies generated by years of studies and reserveassociated concepts. The most striking challenges are the absence of an operational definition of CR and the lack of clarification of its neural bases, the relationship between the brain and CR, and which factors affect brain reserve [19]. Making an effort to overcome these difficulties, a consensus report tried to clarify CR terminology [17] by claiming "resilience" as an umbrella concept that describes the process of coping with age- and disease-related changes, which includes multiple reserve related-concepts, such as brain reserve, brain maintenance, and CR.

Normal aging is characterized by several brain changes at the morphometric and functional level, and associated neuropsychological changes, that are particularly relevant in the frontal lobes on which Executive Functions (EF) heavily depend upon [20]. Among other areas of cognition, EF play a critical role in everyday life, allowing individuals to plan ahead, focus attention, and switch between tasks, hence maintaining effective levels of independent functioning. Variable EF trajectories include

*The Role of Cognitive Reserve in Executive Functioning and Its Relationship to Cognitive Decline… DOI: http://dx.doi.org/10.5772/intechopen.104646*

development into early adulthood and decline into older age, associated with structural and functional changes in the prefrontal cortex [21]. Despite this age-related decline, EF also assumes an important role in maintaining global cognitive efficiency in the late period of life, thanks to a higher CR [22].

There is considerable interest in understanding the processes underlying cognitive decline (and whether they result from specific or general impairments that reflect different patterns and different pathological processes) but also in how the brain actively copes with these deleterious effects on EF so functional independence can be maintained. Next in this chapter, we will review evidence that focuses on certain socio-behavioral CR proxies (e.g., education, occupational complexity, leisure activities, and social involvement), how they may help to cope with age-related changes and brain pathology, and how they relate with EF. Further, differences between "active" versus "passive" models of reserve and the underlying CR mechanism ("neural reserve" vs. "neural compensation") are described.
