Aging is characterized with a time-dependent gradual accumulation of cell damage and continual physiological functional decline. As such, it is also the most profound risk factor for many diseases. Neurodegenerative diseases, such as Alzheimer's, Parkinson's, and Huntington's diseases, as well as sensorial disfunctions all increase considerably upon aging. With the growth in aging population and increasing burden of health care for people with age-related diseases, including AD, intense efforts have been put forth to understand and prevent the effects of aging. The major cellular and molecular hallmarks of aging have been identified and their relationships to age-related diseases, and especially to AD as one of the most common neurodegenerative disorders, have been explored. The hallmarks of aging include a variety of interrelated molecular and cellular mechanisms that act jointly to manage the aging process. Aging has been characterized as a progressive degeneration accompanied by processes like stem cell exhaustion, extracellular matrix modifications, cellular senescence, tissue inflammation, and metabolic dysfunction. These cellular and tissue modifications reflect inherent molecular deviations in mitochondria, epigenetics, DNA maintenance, proteostasis, intercellular interactions, and nutrient sensing, which cause genomic instability and impairment, including telomere dysfunction. DNA damage markers have been found in brain regions of AD patients [26-30], indicating that DNA damage may be an important pathological cause of AD, particularly in lateonset AD cases. Genomic instability impacts the expression of the genes linked to mitochondrial and metabolic dysfunction, altered proteostasis, and age-related inflammation (inflammaging), which are intrinsically involved in aging, and supports the view that DNA damage could be the root of aging and AD. Hence, targeting DNA damage or other aging hallmarks offers an approach to developing treatments to combat age-related diseases, including AD. Telomeres shorten with age, and some 50 nucleotides are lost upon each cell cycle. Neurons, as post-mitotic cells, are not expected to have their telomeres shortened, yet they may still accumulate DNA damage, causing cellular senescence or even apoptosis. Neural stem cells, in contrast, are proliferative and affected by aging, so telomere maintenance is vital for their viability and self-renewal potential, while telomere shortening may trigger cognitive impairment. Epigenetic mechanisms are known to contribute directly to aging and agingrelated diseases. It has been shown that epigenetics play a key role in maintaining genome integrity and regulating gene expression, and its dysfunction is closely related to AD pathogenesis. DNA methylation refers to the attachment of a methyl group to the DNA chain and is considered one of the aging hallmarks. Abnormal DNA methylation has been associated with many AD susceptibility genes, including amyloid precursor protein (APP), β-and γ-secretases, apolipoprotein E, to mention a few. As an organism ages, the proteome, like the genome, is easily damaged, so loss of proteostasis come up another hallmark of aging. At the early and advanced stages of AD, alteration of protein synthesis pathways, including nuclear chaperones, ribosomal proteins, and elongation factors, has been detected in the frontal cortex and hippocampus. Furthermore, proteins associated with various other biological processes are also aberrantly downregulated due to genomic instability in the AD brain. A search in the CAS Content Collection by SciFinder-n 162 for co-occurrence of AD and the aging hallmarks term that AD is most often discussed in the context of mitochondrial dysfunction, impaired autophagy, and lipid metabolism disorders (Figure ). Indeed, mitochondrial dysfunction has been found related to virtually all the associated AD pathologies, including accumulation of plaques and tangles in the hippocampal and cortical neurons of the brain, abnormal microvasculature, interneuron miscommunication, enhanced βamyloid production, elevated inflammatory response, advanced production of reactive oxygen species, impaired brain metabolism, tau hyperphosphorylation, and disruption of acetylcholine signaling. Autophagy is an evolutionarily conserved lysosome-dependent cellular pathway closely related to modulation of protein metabolism, by way of which damaged organelles and misfolded proteins are degraded and recycled to preserve protein homeostasis. Accumulating evidence has revealed that impaired autophagy critically contributes to AD pathogenesis. Immature autophagosome accumulation and dystrophic neurites have been detected in the AD patients brains. Furthermore, the expression of certain autophagy-related proteins has been reported to be downregulated in AD brains. Increasing evidence has recently indicated that dysfunctional autophagy is not just correlated with AD pathologies, but is possibly a causative factor for AD development. Various AD risk genes, including PSEN1, PICALM, CLU, TREM2 have been shown to modulate autophagy. Therefore, promoting autophagy to augment the elimination of misfolded proteins is recommended to be an opportunity for AD therapy. Though the abnormal accumulation of lipids has been described in the very first report of AD neuropathology , it has not been until recently that lipid homeostasis impairment has become a focus of AD research. Lipidomic and metabolomic studies have consistently exhibited alterations in the levels of various lipid classes emerging in early stages of AD brains. Multidimensional interactions between lipid metabolism and key AD pathogenic pathways including amyloidogenesis, bioenergetic deficit, oxidative stress, neuroinflammation, and myelin degeneration have been revealed. With respect to the relative growth in the number of documents correlating AD with various aging hallmarks, telomere attrition exhibits the highest growth, followed by the dysregulated nutrient sensing (Figure ). Indeed, the research of telomere biology is one of the most invested areas of research in AD prevention and treatment, due to its involvement in many age-related diseases. The presence of shorter telomeres in multiple somatic samples from AD patients, especially in leukocytes, has been reported. It has been suggested that the telomere shortening in peripheral leukocytes might be explained by certain known AD features on a molecular level such as high inflammatory cytokine levels and oxidative stress. Deregulated nutrient sensing is increasingly thought to play a role in the pathophysiology of neurodegenerative diseases such as AD. Nutrient sensing is increasingly emerging both as a key modulator of neurogenesis, and, through mTOR, of the autophagic process. The extensive role that deregulated nutrient sensing may play in dementia offers a possible therapeutic pathway, as many nutrient sensing-modulating therapeutics already exist.