Accumulation of modified proteins and aggregate formation in aging

Autofluorescence of Skin Advanced Glycation End Products as a Risk Factor for Open Angle Glaucoma: The ALIENOR Study

“…21,71,72 Indeed, some other fluorophores such as keratin, vitamin D, or lipofuscin, the latter being involved in the aging process as well as in the formation of AGEs, are within the range of excitation light of the AGE-reader. 11 Additionally, some other nonfluorescent chromophores such as melanin or hemoglobin may also have influenced sAF measurements. 73 Our population sample of elderly people has a higher mean age than that observed in other published studies with a cumulative exposure to metabolic activity over a longer period.…”

“…8 Furthermore, they can also influence the incidence or progression of several age-related chronic diseases, such as chronic kidney disease, cardiovascular disease, heart failure, and dementia or other neurodegenerative diseases. [11][12][13][14][15][16] Additionally, some experimental studies have demonstrated that AGEs accumulate in ocular tissues and may be involved in the pathophysiologic process of eye diseases, such as cataract, diabetic retinopathy, or AMD. [17][18][19] Accumulation of AGEs can be estimated with skin autofluorescence (sAF) measurements using a noninvasive device.…”

Exogenous Hsp70 delays senescence and improves cognitive function in aging mice

“…In contrast to synaptophysin, lipofuscin concentration increases with aging. In human brain, lipofuscin is generated and accumulated in neurons as part of the aging process (35). It is hypothesized that prevention of lipofuscin accumulation in the brain will slow aging processes and inhibit the development of neurodegenerative diseases (33,35,36).…”

“…In human brain, lipofuscin is generated and accumulated in neurons as part of the aging process (35). It is hypothesized that prevention of lipofuscin accumulation in the brain will slow aging processes and inhibit the development of neurodegenerative diseases (33,35,36). In previous studies, accumulation of lipofuscin was higher in the hippocampus in comparison with the cortex in aged animals (37).…”

Theories of Human Aging of Molecules to Society

“…Although these systems can eliminate proteolytic modified proteins, it is demonstrated that the activity of these proteases declines with aging, leading to accumulation of damaged tissue proteins and protein aggregates [85]. These enzymatic changes are sufficient to explain how the glycosylation of proteins leads to the lens opacification and cataract formation [11].…”