Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare autosomal dominant genetic disorder of accelerated aging caused by a point mutation in LMNA gene coding for a nuclear protein Lamin A which maintains normal structure and function of the nucleus. Mutated Lamin A protein undergoes a series of enzymatic modifications including farnesylation and prenylation to form a toxic protein progerin that alters nuclear structure and function. HGPS disease begins in utero; however, infants appear normal at birth with some features such as circumoral pallor. The expression of progerin is low in undifferentiated cells which may account for the fewer symptoms of progeria. In about 9-12 months, the levels of progerin in cells become high enough to produce nuclear structure abnormalities leading to cellular and molecular damages characteristic of HGPS. The average age of these patients is 14.6 years. Some therapeutic agents were developed by inhibiting a specific target, such as transcriptional activity, post-translation enzymatic steps, autophagy, and oxidative stress. These agents were tested in experimental models of cells of progeria yielding a modest improvements in phenotypes and slight extension of the lifespan of progeria patients. Since oxidative stress and chronic inflammation are involved in pathogenesis of progeria, this review proposes that a combination of a mixture of micronutrients with currently used therapeutic approaches may extend the life-span more than that produced by drug therapy alone.