Majör depresyon, tıpkı anksiyete gibi, davranı.sal portföyümüzün içerisinde büyük bir yer tutmaktadır Yaklaşık beş kişiden birinde rastlanmasının sebebine, sorumlu patofizyolojik süreçlerin ve modüllerin beynimizde “neden” veya “niçin” var olduklarına ve depresyonun, anksiyetenin, bipolaritenin, hâtta psikotik tabloların neden bu kadar sık ve kom.u spektrumlar içerisinde ortaya çıktığı sorusuna mevcut alışılagelmi. biyolojik, psikolojik ve toplumsal kuramlar yeterli bir açıklama getirememektedir. Evrimsel paradigma, bütün bu sözüm ona çok farklı yakla.ımları kucaklayan yeni bir çerçeve olarak kar.ımıza çıkmaktadır. Bu yaklaşıma göre depresyon evrimsel arketipal adaptif stratejilerin önde gelenlerinden biridir ve klinik tablonun geli.mesinde sitokinlerin hem periferik hem de merkezî mekanizmalarda önemli bir yeri vardır. Bu durum, müstakbel tedavi stratejileri için de yeni bir hedefi işaret etmektedir

Major depression, just like anxiety, has a crucial place in our behavioral portfolio. Neither of the conventional biological, psychological or social theories can explain the innate existence and the causality and finality of responsible brain modules and patho-physiological processes, nor can they explain the high frequency of appearance of anxiety, bipolarity, and psychotic disorders occurring in proximate, sometimes impossible to discriminate, spectra. Evolutionary paradigm appears to be a new frame encompassing all of these so called distinct approaches and psychopathologies. According to evolutionary perspective, depression is one of the most commonly utilized adaptive archetypal strategies and cytokines have essential roles both peripherally (like many interleukins) and centrally (like tumor necrosing factor alpha: TNF-a, and brain derived nerve growth factor: BDNF) in the development of the clinical picture. Drugs like interferon-alpha (a cytokine frequently used for the treatment of multiple sclerosis) commonly cause depression which can be treated or pre-treated with antidepressants. The “sickness behavior” induced by the formation of the cytokines is similar with depression in terms of phenomenology both in animals and in human. Depression, as a behavioral strategy, is both adaptive and it also serves for social signaling and interaction. With the behavioral signaling, depressive individuals inform others that they are in trouble and need help. They also give the message “I am not a source of threat or envy and I am no more a competitor” which in turn, is an equivalent of altruistic behavior. This strategy generally ends up with personal and social adaptation. If it persists beyond its aim and becomes dysfunctional, depression becomes a disorder. This perspective and the role of the cytokines in the pathophysiology of depression may constitute a reasonably good novel target for the present and future treatment strategies.