Abstract
Background and purpose of the studyRecent studies demonstrate that androgens, beyond regulating sexual behavior, exert several neuroprotective functions in the brain. The present study was designed to explore effect of testosterone in memory impairment induced by intra- cerebroventricular (icv) injection of streptozotocin (STZ) as a model of sporadic AD.MethodsStudy was carried out on male Wistar rats. Animals were randomly divided into 11 equal groups. Experimental model of AD was induced by bilateral icv injection of STZ at the dose of 750 μg/Rat/10 μl ACSF at days 1 and 3. STZ-induced memory impairment was assessed two weeks after the last dose of STZ by using a passive avoidance task (1 mA). The interval between the placement of animals in the illuminated chamber and the entry into the dark chamber was measured as a step-through latency (STL). Castration was performed by surgical removing of testis and behavioral study of memory impairment was done after 4 weeks.ResultsResults of this study showed that icv injection of STZ could induce marked (p < 0.05) memory impairment at the dose of 750 μg/Rat/dissolve10 μl CSF/bilateral/days 1 and 3. Therefore, we used this dose of STZ for induction of experimental model of AD. Memory was worsened in castrated rats (P < 0.05) when compared with normal and sham-operated animals. Testosterone replacement therapy (1 mg/kg, sc, for 6 days) in 4 week castrated rats restored memory up to the level of control groups. Testosterone had not any significant effect on memory impairments of non-castrated rats.Major conclusionAccording to the obtained results it can be concluded that testosterone improves cognitive and memory impairment of AD. We suggest that testosterone replacement therapy may have beneficial effect in ameliorating memory impairments of senile patients suffering from AD. Further clinical studies should be carried out to prove possible useful effect of testosterone as an adjuvant therapy in AD.
Highlights
Obesity has reached epidemic proportions and is still escalating at an alarming rate worldwide
Obesity is associated with chronic activation of low-grade inflammation [3], which is implicated in the pathogenesis of obesity-associated diseases including insulin resistance, type-2 diabetes (T2D) [4, 5] and cardiovascular disease [6, 7]
A numerous of studies has been shown that shortchain fatty acids (SCFAs) inhibit inflammation with focus on butyrate and to a lesser extent on acetate and Propionic Acid (PA), [16]
Summary
Obesity has reached epidemic proportions and is still escalating at an alarming rate worldwide. In Palestine the prevalence of obesity has been shown to be approximately 4. The etiology of obesity and low-grade inflammation is complex and involves intrinsic and extrinsic factors. The colonization of germ-free mice with microbiota derived from obese mice results in significantly greater adiposity than colonization with microbiota from lean mice [12]. Prebiotic diets such as fructans [13] are associated with general better health, including the decrease in body weight, fat mass and the severity of T2D [14,15,16]. The factors that influence the composition and metabolism of intestinal
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