## 1 Introduction  
The progressive aging of the world's population and the high impact of major human pathologies, including neurodegenerative diseases, have catalyzed the emergence of new tools that could lead to preventive, early diagnosis, or therapeutic strategies. Alzheimer's disease (AD), the most common neurodegenerative disorder among the elderly, accounts for 60-70% of all dementia cases and carries a high morbidity rate, with serious social and economic consequences [1]. By 2030, it is estimated that approximately 75 million people in developing countries will be affected by AD. While each person experiences biological aging differently, aging is widely recognized as a gradual decline in molecular, cellular, tissue, and, ultimately, organ function, leading to a loss of physiological integrity, which includes the underlying pathology of AD [2]. Despite extensive research on the pathological and clinical aspects of AD, its precise etiology remains unknown due to the disease's heterogeneity and complexity. The hallmarks of AD pathology, namely amyloid-beta (A\(\beta\)) formation and extracellular deposits of plaques and hyperphosphorylated tau protein correlated with neurofibrillary tangles (NFTs), which are linked to synaptic and neuronal loss [3, 4], are now recognized to develop several years before any clinical symptoms become apparent in patients. Despite extensive investigation into the mechanisms behind the pathology of amyloid-beta(A\(\beta\)) plaques, hyperphosphorylated tau aggregates, and neurofibrillary tangles (NFT), a clear understanding of AD's pathogenesis remains elusive, hindering efforts to prevent the disease. In recent years, numerous clinical and research studies have demonstrated the strong correlation between neuroinflammation and neurodegeneration, with a well-balanced innate and adaptive immune system participating in the inflammatory pathways of the central nervous system (CNS) [5; 6]. Neuroinflammation, unlike other risk factors or genetic causes of AD, appears to have a pivotal role as a result rather than as a cause of the AD pathology background. Chronic and persistent activation of the innate immune system of the brain triggers the release and inflammatory cascade of pro-inflammatory and toxic products, such as cytokines and reactive oxygen species, which facilitates the A\(\beta\) and NFT pathologies [7; 8; 9; 10]. The increased presence of pro-inflammatory cytokines, TNF-\(\alpha\), IL-2, IL-1\(\beta\), and IL-6 in the CNS and blood of AD and MCI patients [11] suggests a strong correlation between Alzheimer's disease and MCI patients in a peripheral inflammation state, and its crucial role in the mechanisms associated with aging and neuroinflammation disorders [12]. It is well known that the upregulation of pro-inflammatory cytokines that can affect brain function is a consequence of a chronic low-grade state of inflammation [13; 14; 15]. Proinflammatory cytokines TNFa, IL-1\(\beta\), and IL-6 have been described as having a fundamental role in the integrity of the blood-brain barrier (BBB) and its specific defensive functions. During AD progression, the upregulation of TNF-\(\alpha\) and IL-6 is linked to the alteration of BBB function, facilitating the crossover of lymphocytes and macrophages from the periphery into the brain, supporting the strong relationship between the immune system and central nervous system (CNS) [16; 17; 18]. Aging or peripheral inflammatory conditions can also lead to alterations in the blood-brain barrier, allowing immune cells to enter the brain tissue and potentially supporting neuropathological processes [19; 20] depending on the duration and intensity of stimulation. The in-depth interpretation and translation of these pathological pathways that could form a potential connection between normal aging and risk factors that lead to neuroinflammation and AD is of great importance for prevention and potential lifestyle interventions [21; 22].