Aging is recognized as the leading risk factor for chronic diseases, including Alzheimer's Disease (AD), even as age-specific incidence rates decline in high-income countries.

The World Health Organization forecasts a dramatic increase in dementia cases, projecting the number of individuals living with dementia will rise from approximately 46.8 million in 2015 to 131.5 million by 2050, largely driven by an aging population.

The geroscience hypothesis posits that the aging process heightens vulnerability to chronic diseases, suggesting that interventions aimed at slowing aging could potentially delay the onset of conditions like dementia.

A recent review underscores the intricate relationship between aging and Alzheimer's, calling attention to the necessity for additional research to uncover potential therapeutic targets.

This review specifically analyzes studies that connect biological aging, particularly the twelve hallmarks of aging, with key Alzheimer's biomarkers, namely Aβ and Tau.

López-Otín and colleagues have identified twelve hallmarks of aging, such as genomic instability, telomere attrition, and chronic inflammation, all of which may play a role in the pathogenesis of Alzheimer's Disease.

Research indicates that genomic instability is linked to both Aβ and Tau pathology, with various forms of DNA damage associated with each type of pathology.

Despite the extensive preclinical research conducted, there remains a significant need for more human studies that explore the relationship between aging hallmarks and Alzheimer's Disease.

Recent clinical trials are shifting focus to investigate how medications targeting aging hallmarks can influence core Alzheimer's biomarkers, rather than solely addressing clinical symptoms.

The literature search for relevant studies yielded 3,709 articles, which were subsequently narrowed down to 115 pertinent studies after excluding non-applicable research.