“…In addition to stroke, the efficacy of melatonin in inhibiting oxidative damage has also been tested in a variety of neurological disease models where free radicals have been implicated as being at least partial causal agents of the condition. Thus, melatonin has been shown to reduce Aβ protein toxicity in AD animal models (Dragicevic et al, 2011;Matsubara et al, 2003;Olcese et al, 2009;Pappolla et al, 1997), to reduce oxidative damage in several models of PD (Acuña- Castroviejo-Castroviejo et al, 1997;Chuang and Chen, 2004;Dabbeni-Sala et al, 2001;Jin et al, 1998;Saravanan et al, 2007;Singhal et al, 2010), to protect against glutamate excitotoxicity (Das et al, 2010;Giusti et al, 1996a) and to lower neural damage due to cadmium toxicity (Jiménez-Ortega et al, 2011;Poliandri et al, 2006), δ-aminolevulinic acid toxicity (porphyria) (Carneiro and Reiter, 1998;Onuki et al, 2005;Princ et al, 1997), hyperbaric hyperoxia (Pablos et al, 1997;Shaikh et al, 1997), brain trauma (Beni et al, 2004;Kabadi and Maher, 2010;Tsai et al, 2011), γ radiation (Erol et al, 2004;Shirazi et al, 2011;Taysi et al, 2008), focal ischemia (Kilic et al, 2011;Koh, 2012;Lee et al, 2004;Tai et al, 2011) and a variety of neural toxins (Reiter et al, 2010).…”