In fact, most vital organs and tissues of the body undergo certain age-related decline in function. Thus, muscle strength decays with age, bones weaken losing mass and/or density, skin exhibit visible changes, and also may show signs of impaired wound healing. Blood level of certain hormones (e.g., growth hormone, androsterone, testosterone) decline with age, while others (e.g., gonadotropins, insulin) increase with age. Overall immune function deteriorates, becoming slower to respond, leading to an increased susceptibility to various infectious diseases. Sleep worsens, certain sleep disorders develop. Vision and hearing decline. Kidney tissue decreases and kidney function diminishes, along with multiple other age-related changes. The efforts to understand and prevent the effects of aging date back centuries, so the anti-aging research has a long history (Figure ). In ancient times many cultures developed traditional remedies and practices aimed at promoting longevity and slowing the aging process. For example, ancient Chinese medicine includes herbal remedies and acupuncture techniques designed to promote health and longevity. In 16th century Italian physician and philosopher Girolamo Cardano wrote a treatise on aging and longevity, in which he discussed the physical and mental changes that occur with age and proposed strategies for promoting health and extending lifespan. In 19th century, French physiologist Claude Bernard proposed that aging is caused by changes in the internal ambiance of the body, including changes in metabolism and the accumulation of toxins. In the early 20th century, scientists began to study the effects of diet and lifestyle on aging, with researchers like Elie Metchnikoff proposing that the gut microbiome plays a role in aging. The free radical theory of aging was proposed by Denham Harman, who suggested that aging is caused by damage to cells and tissues by unstable molecules called free radicals. Figure . Timeline of key events and discoveries in anti-aging research. An early step in the field of aging exploration has been the observation that restriction of caloric intake increases lifespan -first demonstrated in mice and rats , and later in other species as well, including primates. Moreover, it was detected that dietary restrictions enhanced not only the lifetime but also the healthspan, suppressing the development of age-related diseases. Thus, a concept emerged that correlation exists between lifespan and healthspan, described as the portion of lifespan free from disease. Mutation accumulation theory that aging is a result of decline in the power of natural selection after reproduction was proposed in 1952. Over 30 years later, landmark research in the nematode Caenorhabditis elegans demonstrated that the mutant nematode strain exhibits a 40-60% extended lifespan, showing that a single gene, the AGE-1 gene, can control the lifespan of an organism. The close link between telomeres and aging originates in the discovery of a unique structure at the last portions of the Zea mays and Drosophila melanogaster chromosomes, hypothesized to play a significant role in preventing chromosome end fusion. In the early 1960s, Hayflick noted that human cells in tissue culture cease dividing after a certain number of cell divisions by a process termed replicative senescence. It was shown later that human fetal cells exhibited finite replication potential of 50-60 doublings, labelled as replicative senescence or the ''Hayflick limit". The link between the ending of cell division and replication of telomeres was revealed in the early 1970s. It was established that telomere attrition takes place in parallel with the replication lifespan of human primary cells, thus demonstrating that shortened telomeres cause the Hayflick limit. It took nearly two decades for the suggested causative relationship between replication senescence and telomere shortening to be established. Thus, the aging of cells could be associated with alterations in telomere length on genomic DNA. Further on, via animal models, the function of telomeres in aging was authenticated and identified as an essential signaling pathway guiding the aging process Telomere dysfunction was shown to accelerate signs and symptoms of aging. Later, transcriptomic studies revealed the p53 aging pathway, promoting apoptosis, thus integrating three previously distinct theories of aging: genotoxicity (telomere dysfunction), oxidative damage, and mitochondrial decay. Reactivation of endogenous telomerase, an enzyme that could extend telomere sequence, was demonstrated to reverse advanced premature aging in mice. Noteworthy, adenoviral delivery of telomerase in aged mice was demonstrated to enhance cardiac function after acute myocardial infarction, improve muscle coordination and kidney and liver performance, reduce insulin resistance and subcutaneous fat reduction, increase bone mineral density, and extend life expectancy without triggering a growth in cancer frequency. In the early 1990s, the potential of human growth hormone (hGH) as an anti-aging agent acting to increase lean body mass, decrease adipose tissue mass, and increase bone mineral density was reported , and hGH supplements became available, sparking controversy questioning their safety and effectiveness. Later on, aging research was focused on the genetic pathways of aging, revealing a complex system of intracellular signaling pathways and higher-order processes. Throughout the 1990s, researchers identified genes that are linked to aging, including the SIRT1 gene. A substantial attention to sirtuins was attracted after it was reported that overexpression of SIR2 gene can prolong yeast lifespan by as much as 70%. In the 2000s, advances in biotechnology and genetics lead to the development of new anti-aging therapies, including stem cell therapy, gene therapy, and telomerase activation. In the 2010s and 2020s, the focus of anti-aging research shifted towards advanced understanding of the mechanisms of aging and developing interventions that can slow or reverse the aging process, with ongoing studies exploring a range of potential interventions, including senolytics (drugs that clear out senescent cells), metformin (a diabetes drug that may have anti-aging properties), and various forms of gene therapy. Advances in gene editing technology, such as CRISPR/Cas9, allow for more precise manipulation of genes involved in the aging process. It is important to note that while anti-aging research has made significant strides over the years, most of these researches are still in the non-human systems and there is still much that is not yet understood about the aging process and how to effectively prevent or reverse its effects.