The androchronogenetic
alopecia (AGA) mouse if a mutant strain which expresses
androgen-dependent
baldness. Daily s.c. injection of
testosterone (T) induced thinning of the hair coat along the upper dorsum after 4 weeks of treatment. After 12 to 14 weeks this
diffuse alopecia eventually eveloped into a bald area which extended to the middorsum.
Dihydrotestosterone was more effective than T in stimulating the onset of AGA. In this model, T produced the
alopecia by decreasing the rate of hair growth, decreasing the duration of anagen, and markedly prolonging the duration of telogen. When applied topically at a concentration of 5%,
cyproterone acetate delayed the progression of the T-mediated
hair loss. However, this inhibitory effect occurred through systemic means as evidenced by decrease in the size of the submaxillary gland. Chronic feeding of
androgen-treated female AGA mice with a diet containing 0.01%
minoxidil also inhibited the development of
alopecia. Skin and core temperatures were found to be higher in
minoxidil-treated animals than in the placebo-treated controls.
Minoxidil at a topical dose of 1% did not produce any effect. Increasing the dose to 2% caused a slight retardation of the development of
alopecia. However, a 60% inhibition was observed at a topical dose of 5%
minoxidil after 12 weeks of treatment (p less than 0.03). The data demonstrate that
hair loss in the AGA mouse is
androgen dependent and that this mutant strain can serve as a suitable model for the screening of compounds, such as
antiandrogens and
vasodilators, which may influence the balding process.