Schizophrenia and Mitochondrial Dysfunction

Yıl 2014, Cilt: 6 Sayı: 4, 340 - 354, 06.11.2014

Süleyman Akarsu

https://doi.org/10.5455/cap.20140121114707

Öz

Genetic factors play an important role in the development of schizophrenia that the etiology is clearly not known. However, specific inheritance mechanism of this disorder is still unclear. Inheritance of schizophrenia is thought to be polygenic or multifactorial. In the recent studies, mitochondrial function and cerebral energy metabolism abnormalities have been identified in patients with schizophrenia. Cognitive deficits and behavioral abnormalities evident as typically found in the clinical course of schizophrenia may develop due to the affection of neuronal plasticity and brain circuits by impaired function of mitochondria. Some changes were found in patients with schizophrenia compared with control subjects in the researches examining both brain and peripheral tissues. Also, it was seen that antipsychotics used in the treatment of schizophrenia might lead to a progressive reduction in oxidative phosphorylation capacity of mitochondria by inhibition of respiratory chain. Especially the findings of the peripheral tissues in patients with schizophrenia were considered to be used as a biological marker for schizophrenia in these studies. Changes in the mitochondria of platelets are considered as a peripheral model for the neurons because of the lack of the platelets' own DNA. These changes reflect the findings of the brain in a variety of neuropsychiatric disorders. At the present time, making the diagnosis of schizophrenia based on only clinical criteria reveal the necessity of finding peripheral biological marker for schizophrenia. Thus further systematic studies investigating the relationship between schizophrenia and changes in mitochondrial electron transport chain are required.

Anahtar Kelimeler

Schizophrenia, mitochondrial dysfunction, biological marker

Şizofreni ve Mitokondrial Disfonksiyon

Öz

Etyolojisi net olarak bilinmeyen şizofreninin oluşumunda genetik faktörler önemli rol oynamaktadır. Ancak, bu bozukluğun spesifik kalıtımsal mekanizması henüz açıklanamamıştır. Şizofreni kalıtımının poligenik veya multifaktöryel olabileceği düşünülmektedir. Son dönemde yapılan çalışmalarda, şizofreni olgularında mitokondrial fonksiyon ve serebral enerji metabolizmasında anormallikler tespit edilmiştir. Mitokondri fonksiyonlarındaki bozulma ile nöronal plastisite ve beyin devreleri etkilenerek, şizofreninin klinik tablosunda da belirgin olarak rastlanabilen davranış anormallikleri ve bilişsel defisitler gelişebilir. Şizofreni olgularının hem beyin hem de periferal dokularının incelendiği araştırmalarda, şizofreni olgularında sağlıklı olgulara göre bazı değişiklikler saptanmıştır. Ayrıca şizofreni tedavisinde kullanılan antipsikotiklerin solunum zinciri inhibisyonu yaparak mitokondrinin oksidatif fosforilasyon kapasitesinde progresif olarak azalmaya neden olabileceği görülmüştür. Bu çalışmalarda, özellikle periferal dokulardan elde edilen bulguların, şizofreni tanısında biyolojik bir belirteç olarak kullanılabileceği önerilmiştir. Plateletlerin kendi DNA'sı olmadığı için, platelet mitokondrisinde gerçekleşen değişiklikler nöronlar için periferal bir model olarak kabul edilmektedir. Bu değişiklikler çeşitli nöropsikiyatrik rahatsızlıklarda beyindeki bulguları yansıtmaktadır. Günümüzde şizofreni tanısının klinik ölçütlere dayalı olması, şizofreni için periferal biyolojik bir belirteç gerekliliğini ortaya koymaktadır. Bu nedenle mitokondrial elektron transport zincirindeki değişikliklerin şizofreni ile ilişkisini araştıran daha sistematik çalışmaların yapılması gereklidir.

Anahtar Kelimeler

Şizofreni, mitokondrial disfonksiyon, biyolojik belirteç

Kaynakça

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• Süleyman Akarsu, Uzm.Dr., Aksaz Asker Hastanesi, Marmaris Yazışma Adresi/Correspondence: Süleyman Akarsu, Aksaz Asker Hastanesi, Marmaris, Turkey. E-mail: [e-mail] Yazarlar bu makale ile ilgili herhangi bir çıkar çatışması bildirmemiştir. The authors reported no conflict of interest related to this article. Çevrimiçi adresi / Available online at: www.cappsy.org/archives/vol6/no4/ Çevrimiçi yayım / Published online 21 Ocak/January 21, 2014; doi: 10.5455/cap.20140121114707