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Background: It has been studied that nutrition can influence Alzheimer’s disease (AD) onset and progression. Some studies on rodents using intraventricular streptozotocin (STZ) injection showed that this toxin changes cerebral glucose metabolism and insulin signaling pathways. Objective: The aim of the present study was to evaluate whether a nutritional formulation could reduce cognitive impairment in STZ-induced animals. Methods: The rats were randomly divided into two groups: sham and STZ. The STZ group received a single bilateral STZ-ICV injection (1 mg/kg). The sham group received a bilateral ICV injection of 0.9% saline solution. The animals were treated with AZ1 formulation (Instanth® NEO, Prodiet Medical Nutrition) (1 g/kg, PO) or its vehicle (saline solution) for 30 days, once a day starting one day after the stereotaxic surgery (n = 6–10). The rats were evaluated using the open field test to evaluate locomotor activity at day 27 after surgery. Cognitive performance was evaluated at day 28 using the object recognition test and the spatial version of the Y-maze test. At day 30, the rats were anesthetized with chloral hydrate (400 mg/kg, i.p) and euthanized in order to evaluate IBA1 in the hippocampus. The differences were analyzed using one-way ANOVA with Bonferroni’s or Kruskal Wallis with Dunn’s post-hoc test. Results/Conclusion: STZ-lesioned rats present memory impairment besides the increased microglial activation. The treatment with AZ1 formulation reversed the memory impairment observed in the object recognition test and Y-maze and also reduced IBA1 in CA1 and DG.

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Background: Alzheimer’s disease (AD) is the most common cause of dementia in the elderly and is characterized by progressive cognitive decline. Considerable evidence supports an important role of amyloid-β oligomers (AβOs) in the pathogenesis of AD, including the induction of aberrant glial activation and memory impairment. Objective: We have investigated the protective actions of a nutritional formulation, denoted AZ formulation, on glial activation and memory deficits induced by intracerebroventricular (i.c.v.) infusion of AβOs in mice. Methods: Two-month-old male mice were treated orally with AZ formulation or isocaloric placebo for 30 consecutive days. Microglial and astrocytic activation were analyzed by immunohistochemistry in the hippocampus 10 days after i.c.v. infusion of AβOs (n = 5 mice per experimental condition). Memory loss was assessed by the novel object recognition (NOR) test (n = 6–10 mice per experimental condition). Results: Oral treatment with the AZ formulation prevented hippocampal microglial and astrocytic activation induced by i.c.v. infusion of AβOs. The AZ formulation further protected mice from AβO-induced memory impairment. Conclusion: Results suggest that administration of the AZ formulation may comprise a promising preventative and non-pharmacological strategy to reduce brain inflammation and attenuate memory impairment in AD.

To assess the glycaemic response after ingestion of two specialised oral and enteral nutrition formulas for glycaemic control. The participants were 16 healthy volunteers, aged 21 to 49 years old, with normal glucose tolerance. The volunteers attended the tests fasting for 10 hours, for 5 weeks, and consumed the reference food – glucose solution – for 3 weeks, and the two formulas DiamaxO and DiamaxIG in the following weeks, in amounts equivalent to 25g of available carbohydrates. During the period of 120 minutes, seven blood samples were taken through capillary blood sampling to determine the glycaemic response. The glycaemic index (GI) was calculated according to the trapezoidal rule, ignoring areas below the fasting line. The glycaemic load (GL) was determined by the formula GL=[(GI(glucose=reference) X “g” of available carbohydrate per serving]/100. The formulas showed low GI and GL. GI=37.8 and GL=6.6 for DiamaxO and GI=21.5 and GL=3.5 for DiamaxIG. The peak of the glycaemic response occurred 30min after ingestion, with a marked difference in blood glucose between the Diamax products in relation to glucose. Differences were also significant at times 15, 45, 60 and 90 minutes in relation to glucose (ANOVA with post hoc Bonferroni, p<0.005), but not between the two products. However, the area under the curve and the GI of DiamaxIG is significantly smaller than that of the DiamaxO second t test (p=0.0059). The glycaemic response to the products is quite reduced, presenting a curve with a little accentuated shape, without high peak, especially in the modified product.