Long-term oral galactose treatment prevents cognitive deficits in male Wistar rats treated intracerebroventricularly with streptozotocin

Šalković‐Petrišić, Melita; Osmanovic-Barilar, Jelena; Knezović, Ana; Hoyer, Siegfried; Mosetter, Kurt; Reutter, Werner

doi:10.1016/j.neuropharm.2013.09.002

Cited by 73 publications

(86 citation statements)

References 97 publications

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“…23 Still, a review of published papers shows that there is no consensus concerning the dosage, age, strain of mice and rats, and time interval. 15,17,19 For example, different strains of mice and rats are used, the injection dose varies between 50 mg/kg to 1250 mg/kg and the period of injection varies from 6 to 12 weeks or more. 15,17 The administration can be i.p., s.c., or oral.…”

Section: Discussionmentioning

confidence: 99%

“…16,17 It is important to note that, more recently, some dissonant reports concerning the effectiveness of this accelerated aging paradigm have been published. [18][19][20] Indeed, Parameshwaran and collaborators have concluded that the d-galactose treatment (intraperitoneal [i.p] injection of 100 mg/kg per day) in female C57BL/61 mice was not suitable for testing antioxidant compounds in mice. 18 Moreover, Tikhonova and collaborators found that d-galactose treatment (i.p.…”

Section: Introductionmentioning

confidence: 99%

“…20 Likewise, Salkovic-Petresic and collaborators found that 1-month oral galactose treatment (200 mg/kg per day) failed to induce changes in the spatial memory of male Fisher and female Wistar rats. 19 Several factors could be at the base of the apparent lack of congruence of d-galactose as an accelerated aging model. For instance, as in normal aging 21,22 gender also appears to be an important factor in accelerated senescence induction.…”

Section: Introductionmentioning

confidence: 99%

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d-Galactose High-Dose Administration Failed to Induce Accelerated Aging Changes in Neurogenesis, Anxiety, and Spatial Memory on Young Male Wistar Rats

Cardoso

Magano

Marrana

et al. 2015

Rejuvenation Research

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The model of accelerated senescence with the prolonged administration of d-galactose is used in anti-aging studies because it mimics several aging-associated alterations such as increase of oxidative stress and decline of cognition. However, there is no standardized protocol for this aging model, and recently some reports have questioned its effectiveness. To clarify this issue, we used a model of high-dose d-galactose on 1-month-old male Wistar rats and studied the hippocampus, one of the most affected brain regions. In one group (n = 10), d-galactose was daily administered intraperitoneally (300 mg/kg) during 8 weeks whereas age-matched controls (n = 10) were injected intraperitoneally with saline. A third group (n = 10) was treated with the same dose of d-galactose and with oral epigallocatechin-3-gallate (EGCG) (2 grams/L), a green tea catechin with anti-oxidant and neuroprotective properties. After treatments, animals were submitted to open-field, elevated plus-maze and Morris water maze tests, and neurogenesis in the dentate gyrus subgranular layer was quantified. There were no significant alterations when the three groups were compared in the number of doublecortin-and Ki-67-immunoreactive cells, and also on anxiety levels, spatial learning, and memory. Therefore, d-galactose was not effective in the induction of accelerated aging, and EGCG administered to d-galactose-treated animals did not improve behavior and had no effects on neurogenesis. We conclude that daily 300 mg/kg of d-galactose administered intraperitoneally may not be a suitable model for inducing age-related neurobehavioral alterations in young male Wistar rats. More studies are necessary to obtain a reliable and reproducible model of accelerated senescence in rodents using d-galactose.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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d-Galactose High-Dose Administration Failed to Induce Accelerated Aging Changes in Neurogenesis, Anxiety, and Spatial Memory on Young Male Wistar Rats

Cardoso

Magano

Marrana

et al. 2015

Rejuvenation Research

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“…This disease exhibits metabolic abnormalities, such as glucose metabolism impairment, abnormal insulin receptor signaling, insulin resistance, oxidative stress, and structural abnormalities in proteins (18). Moreover, dementia in sporadic AD type is associated with dysfunction of the insulin receptor followed by decreased glucose transport via glucose transporter 4 (GLUT-4) and decreased glucose metabolism in brain cells (45).…”

Section: Introductionmentioning

confidence: 99%

Intranasal insulin treatment improves memory and learning in a rat amyloid-beta model of Alzheimer’s disease

Farzampour¹,

Majdi²,

Sadigh-Eteghad³

2016

Physiology International

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Recently, insulin has been used as a pro-cognitive agent for the potential treatment of Alzheimer's disease (AD), because of its ability to cross the brain-blood barrier (BBB) by a saturable transport system. This study has been designed to evaluate the effects of intranasal insulin regimen, as a bypass system of BBB, on spatial memory in amyloid-beta (Aβ) model of AD in rat. Unilateral infusion of Aβ 25-35 (10 nmol/2 μl/rat) into the lateral ventricular region of brain was used to produce a rat model of AD. After a 24-h recovery period, rats received insulin or vehicle via intraperitoneal or intranasal route (0.1, 0.2, and 0.3 IU) for 14 days. Memory function in rats was assessed by Morris water maze test, with 5 days of training and consequent probe test protocol. Different doses of intraperitoneal insulin did not have a significant effect on learning and memory in AD rats. However, intranasal insulin at doses of 0.2 and 0.3 IU improved the learning and memory in Aβ-received rats.In conclusion, intranasal insulin as a non-invasive strategy improves spatial learning and memory in AD model.

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“…For example, studies have been reported the immunostimulatory and antitumor activities of glucans and mannans [4]. Galactose may prevent cognitive deficits associated with glucose hypometabolism in Alzheimer's disease [5]. Recent studies have also focused on the effect of glucans on redox balance [6].…”

Section: Introductionmentioning

confidence: 99%

Analysis and glycosyl composition of the exopolysaccharide isolated from submerged fermentation of Ganoderma lucidum CG144

et al. 2014

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The evaluation of glycosyl composition is an essential step to guide future research designs applied in bioactivity. In the same way, the unexplored potential bioactivity of exopolysaccharide from Ganoderma lucidum is huge. Therefore, this study investigated the glycosyl composition of the exopolysaccharide isolated from submerged fermentation of G. lucidum to serve as guide for future studies on bioactivity. Glycosyl content and composition were evaluated by combined GC/ MS of the TMS derivatives of the monosaccharide methyl glycosides produced from the sample by acidic methanolysis. Glycosyl composition analysis showed that the dominant carbohydrate component in all samples of exopolysaccharide isolated from submerged fermentation of G. lucidum CG 144 was glucose (58.1%), mannose (26.6%) and galactose (12.5%) which can be referred to as heteroglycan. These results suggest that this Ganoderma exopolysaccharide may be a new immunomodulatory agent.

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Long-term oral galactose treatment prevents cognitive deficits in male Wistar rats treated intracerebroventricularly with streptozotocin

Cited by 73 publications

References 97 publications

d-Galactose High-Dose Administration Failed to Induce Accelerated Aging Changes in Neurogenesis, Anxiety, and Spatial Memory on Young Male Wistar Rats

d-Galactose High-Dose Administration Failed to Induce Accelerated Aging Changes in Neurogenesis, Anxiety, and Spatial Memory on Young Male Wistar Rats

Intranasal insulin treatment improves memory and learning in a rat amyloid-beta model of Alzheimer’s disease

Analysis and glycosyl composition of the exopolysaccharide isolated from submerged fermentation of Ganoderma lucidum CG144

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