http://www.ijtrichology.com/article.asp?issn=0974-7753;year=2009;volume=1;issue=1;spage=6;epage=14;aulast=Trueb
L'aticolo è del grande Trueb (in ambito dermatologico-tricologico è come dire R. Paus, Sawaya ecc...)
Though AGA may manifest as early as at the age of 16 years (before 16 years, it is called by definition premature alopecia), balding has traditionally been considered as an attribute of ageing at all times and in all cultures. Indeed, evidence is emerging that AGA may be considered a form of organ-specific premature ageing.
Nevertheless, the limited success rate of treatment of AGA with hair growth promoters, such as topical minoxidil, or modulators of androgen metabolism, such as finasteride, means that further pathogenic pathways must be taken into account.
Recent studies have focused on oxidative stress: Naito et al.[23] have recently analyzed the effect of the lipid peroxides on hair follicles, and observed that the topical application of linolein hydroperoxides http://images.google.it/imgres?imgurl=http://www.caymanchem.com/images/catalog/screen/89430.png&imgrefurl=http://www.caymanchem.com/app/template/Product.vm/catalog/89430/a/z&usg=__8YV8XxgYM9Aphk96Fm1uqINRscU=&h=287&w=960&sz=69&hl=it&start=1&sig2=QSMs7vhx_0t6Chp0DQpbPQ&um=1&tbnid=07ZQrjx3-GBGDM:&tbnh=44&tbnw=148&prev=/images%3Fq%3Dlinolein%2Bhydroperoxides%26hl%3Dit%26sa%3DN%26um%3D1&ei=gthJS4iQEM-9_QaL3aiOAg , one of the lipid peroxides, lead to the early onset of the catagen phase in murine hair cycles. Furthermore, they found that lipid peroxides induced apoptosis of hair follicle cells. They also induced apoptosis in human epidermal keratinocytes by up- regulating apoptosis-related genes. These results indicate that lipid peroxides, which can cause free radicals, induce the apoptosis of hair follicle cells, and this is followed by early onset of the catagen phase. Bahta et al.[24] cultured dermal hair papilla cells (DPC) from balding and nonbalding scalp and demonstrated that balding DPCs grow slower in vitro than nonbalding DPCs. Loss of proliferative capacity of balding DPCs was associated with changes in cell morphology, expression of senescence-associated beta-galactosidase, decreased expression of proliferating cell nuclear antigen and Bmi-1, upregulation of p16 (INK4a)/pRb and nuclear expression of markers of oxidative stress and DNA damage including heat shock protein-27, super oxide dismutase catalase, ataxia-telangiectasia-mutated kinase (ATM), and ATM- and Rad3-related protein. The finding of premature senescence of balding DPC in vitro in association with expression of p16(INK4a)/pRB suggests that balding DPCs are particularly sensitive to environmental stress.