INTRODUCTION
Skin aging is a progressive process that impacts all physiological functions that are important for homeostasis and is the sum of intrinsic (chronological) and extrinsic (photo-aging) aging.1,2
Characteristic clinical features of intrinsically aged skin are the loss of elasticity and the appearance of fine wrinkles, crepiness, and sallowness. This is borne out microscopically by epidermal and dermal atrophy, which diminishes the biomechanical properties of the skin.3
Glycation plays a prominent role in intrinsic skin aging and has been implicated in the progression of various diseases, including chronic diseases such as diabetes, Alzheimer's disease, etc.6 Because of its role in skin aging, glycation is a key anti-age strategy of great importance to cosmeceutical and pharmaceutical companies and is the subject of the present clinical study.
Glycation is a non-enzymatic reaction of a sugar, usually glucose, with lipids, proteins, or DNA. This process is known as the Maillard reaction.7 The electrophilic carbonyl group of the reducing sugar reacts with free amino groups in the amino acids of proteins to form an unstable Schiff base. Further reactions result in the formation of more stable Amadori products.
The principal protein in the dermis is collagen; thus, it is a main target for glycation. The glycation products collectively are called advanced glycation end-products (AGE) and are not degradable. Thus, they accumulate with time and modify the structural properties of collagen. AGEs in the dermis play a role in intrinsically aged skin by disrupting the normal function of the dermis, which results in loss of elasticity and firmness and causes crepiness and sallowness.8 The aforementioned signs of aging are most prevalent among Baby Boomers, currently those aged 61 to 79 years (born 1946-1964).9-11