Intracerebroventricular injection of streptozotocin in rats produces both oxidative stress in the brain and cognitive impairment

LX2343 alleviates cognitive impairments in AD model rats by inhibiting oxidative stress-induced neuronal apoptosis and tauopathy

“…LX2343 ameliorated learning and memory impairments in ICV-STZ rats ICV injection of rats with a sub-diabetogenic dose of STV has been shown to be closely linked to the sporadic dementia of Alzheimer's disease [34] , which is characterized by cognitive impairment [35] , OS [35] , impaired glucose metabolism [36] , and hyperphosphorylated tau [37] . Given the pathological features of ICV-STZ rats and the efficiency of LX2343 in both protecting neuronal cells and attenuating tau pathology, we performed the MWM assay to examine the potential of LX2343 in the amelioration of memory impairment in ICV-STZ rats.…”

Role of GSK3<i>β</i> and PP2A on Regulation of Tau Phosphorylation in Hippocampus and Memory Impairment in ICV-STZ Animal Model of Alzheimer’s Disease

“…produced increase of tau phosphorylation in the brain of non-transgenic mice [7]. Likewise, the ICV administration of low STZ doses (1 -3 mg/kg) reproduces aspects of SAD abnormalities, including decreased glucose utilization in rat cortical regions and hippocampus [24] [25] [26] [27], cholinergic deficits [25], increase in oxidative stress [28] [29] [30], decrease of IR expression and hyperphosphorylated tau protein in the hippocampus [31], and amyloid formation in leptomeningeal vessels [30]. All these changes are associated to memory impairment, and tau pathology, resulting in central insulin dysfunction [30] [31] [32] [33].…”

Multi-target iron-chelators improve memory loss in a rat model of sporadic Alzheimer's disease

“…Animal model which develops insulin resistant brain state and glucose hypometabolism following the intracerebroventricular application of a betacytotoxic drug streptozotocin in small rodents and cynomolgus monkey (STZ-icv model), (Agrawal et al 2011;Grünblatt et al 2007;Lannert and Hoyer 1998;Lee et al 2014;Lester-Coll et al 2006;Plaschke and Hoyer 1993;Salkovic-Petrisic et al 2006), shares similarities with the human sAD condition (Lannert and Hoyer 1998) since insulin resistant brain state was found postmortem in sAD patients (Correia et al 2011;de la Monte and Wands 2005;Frölich et al 1998). Additionally, STZ-icv model demonstrates also cognitive deficits (Mayer et al 1990;Lannert and Hoyer 1998) and decrement in cerebral cholinergic transmission (Blokland and Jolles 1993;Hellweg et al 1992), as well as other features of chronic neurodegeneration like oxidative stress and neuroinflammation (Saxena et al 2011;Sharma and Gupta 2001) and in particular tau protein hyperphosphorylation (Grünblatt et al 2007;Deng et al 2009;Liu et al 2014;Peng et al 2013), pathological Aβ accumulation (Shingo et al 2013) and cerebral amyloid angiopathy (Salkovic-Petrisic et al 2006, 2011.…”