Alopecia Areata (AA) is an autoimmune disorder that is characterized by hair loss on both a patient’s scalp and body. This hair loss can come in the form of patchy hair loss on the scalp (areata, also called AA patchy persistent), total hair loss on the scalp (totalis), and complete loss of all body hair (universalis). While each form of AA is diagnosed separately, the basic mechanism by which the autoantibodies are generated remains the same. Once generated, these antibodies are involved in creating an immune response that eventually attacks a healthy hair follicle, causing irritation of the hair follicle and thus hair loss. The hair follicle, however, is not permanently destroyed and has the ability to re-grow the hair that was once lost. This is especially true in the case of patchy hair loss, as hair can go through cycles of falling out and growing back in, sometimes changing the shape and location of the patches. While there have been some links between AA and other disorders, the majority of patients see no side effects other than hair loss.
Fig 1: Images showing Alopecia Areata (AA pathcy persistent) during multiple stages of of hair loss and regrowth. (Personal Images)
In recent research, there has been a link between oxidative stress and the response of autoantibodies in Alopecia patients. The theory here is that the red blood cells, also known as erythrocytes, of Alopecia patients are subjected to more oxidative stress that can damage proteins and DNA within these red blood cells. One specific consequence of this stress has been noted. The enzyme superoxide disumatse (SOD) is often modified by nitric oxide (NO), which reduces its overall activity. This is important because SOD’s role is to destroy the Reactive Oxygen Species (ROS) that are produced through the normal function of the mitochondria, the source of energy production in cells. Research has shown that antiobodies purified from AA patients have a strong affinity to recognize NO-modified SOD from erythrocytes, pointing to a possible source of initiation or progression of AA.
Fig. 2: A simple representation of oxidative stress (Google Images)
The immune response that results in hair loss has been studied in recent years, and has proved to be very complicated. Researchers have identified a positive feedback loop that results in extensive proliferation of T cells which accumulate at the base of the hair follicle and cause hair loss. Only within the past year has enough information been gathered to produce a useful treatment for AA. Normally, patients were treated in a number of different ways which ranged from experimental steroid injection to the use of over-the-counter hair recovery methods like Rogaine Foam. Most of these treatments, however, proved to be highly ineffective. Interestingly, an existing arthritis medication, Tofacitinib, has been shown to regrow hair in both mouse and human patients by inhibiting a family of proteins called Janus Kinases that are directly involved in the signaling pathway of AA. This is an important step forward that will hopefully result in more effective treatments and a greater understanding of AA and possibly other autoimmune disorders.