Burden of Hair Loss: Stress and the Underestimated Psychosocial Impact of Telogen Effluvium and Androgenetic Alopecia

Hair loss, as it occurs with telogen effluvium and androgenetic alopecia, provokes anxieties and distress more profound than its objective severity would appear to justify. This reflects the profound symbolic and psychosocial importance of hair. Stress has long been implicated as one of the causal factors involved in hair loss. Recently, in vivo studies in mice have substantiated the long-held popular belief that stress can exert profound hair growth-inhibitory catagen-inducing and hair-damaging pro-inflammatory effects. Insights into the negative impact of stress on hair growth and the integration of stress-coping strategies into the management of hair loss disorders as well as the development of new pharmacotherapeutic strategies might lead to enhanced therapeutic modalities with the alleviation of clinical symptoms as well as the concomitant psychological implications

New Roles for Glial Cell Line-Derived Neurotrophic Factor and Neurturin : Involvement in Hair Cycle Control

Glial cell line-derived neurotrophic factor (GDNF), neurturin (NTN), and their receptors, GDNF family receptor α-1 (GFRα-1) and GDNF family receptor α-2 (GFRα-2), are critically important for kidney and nervous system development. However, their role in skin biology, specifically in hair growth control, is as yet unknown. We have studied expression and function of GDNF, neurturin, GFRα-1, and GFRα-2 in murine skin during the cyclic transformation of the hair follicle (HF) from its resting state (telogen) to active growth (anagen) and then through regression (catagen) back to telogen. GDNF protein and GFRα-1 messenger RNA are prominently expressed in telogen skin, which lacks NTN and GFRα-2 transcripts. Early anagen development is accompanied by a significant decline in the skin content of GDNF protein and GFRα-1 transcripts. During the anagen-catagen transition, GDNF, GFRα-1, NTN, and GFRα-2 transcripts reach maximal levels. Compared with wild-type controls, GFRα-1 (+/−) and GFRα-2 (−/−) knockout mice show a significantly accelerated catagen development. Furthermore, GDNF or NTN administration significantly retards HF regression in organ-cultured mouse skin. This suggests important, previously unrecognized roles for GDNF/GFRα-1 and NTN/GFRα-2 signaling in skin biology, specifically in the control of apoptosis-driven HF involution, and raises the possibility that GFRα-1/GFRα-2 agonists/antagonists might become exploitable for the treatment of hair growth disorders that are related to abnormalities in catagen development

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