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Prodiet at ASPEN 2021. Honorable Participation and a Reason to Celebrate

The Prodiet scientific team was once again at the American Society for Enteral and Parenteral Nutrition Congress – ASPEN 2021, from March 20 to 23. On this occasion, the new results from the pre-clinical research in a mouse model of Alzheimer’s Disease, were presented in partnership with UFRJ and researchers Sergio Ferreira and Luciana Siqueira*.

Prodiet at ASPEN 2021

ASPEN 2021

At last year’s congress, the previous results of the research demonstrated that the supplementation with a combination of nutrients: capric and caprylic acid, phosphatidylserine, DHA, and some vitamins and minerals; prevent cognitive damage in this mouse model of the disease.

This year, it demonstrated the probable mechanism by which this combination of nutrients has cognitive benefits. The results pointed to an anti-inflammatory action on the animal’s brains. This finding is significant since neuroinflammation is a central feature of Alzheimer’s Disease pathogenesis.

At last year’s congress, the research awarded as Best International Abstract, and it received an award again. Now, as International Poster of Distinction. We, from the Prodiet team, are happy when we contribute to Science.

Understand the award-winning research, at ASPEN 2021, as “International Poster of Distinction.”

A specialized nutritional formulation reduces hippocampal inflammation induced by intracerebroventricular infusion of amyloid‐β peptide oligomers (AβOs) in mice.

Purpose:

Glucose hypometabolism and amyloid‐β (Aβ) deposition are hallmarks of Alzheimer’s disease (AD), along with brain oxidative stress, lipid peroxidation, and neuroinflammation, culminating in synapse failure and cognitive impairment. Intracerebroventricular (i.c.v.) infusion of amyloid‐β oligomers (AβOs) comprises a well‐established acute mouse model of AD that induces AD‐related neuropathological changes and memory deficit, which can be verified from 24 hours post‐infusion and persists for at least 3 weeks. Our previous data showed that a nutritional formulation (referred to as AZ), which provides ketone bodies as an alternative source of energy along with additional antioxidant and anti‐inflammatory nutrients, prevents memory deficit induced by AβOs. It is well known that AβOs trigger neuroinflammation and microglial activation in the hippocampus, and this plays an important role in cognitive impairment. Thus, the aim of this study was to investigate the effects of AZ treatment on hippocampal microglial activation induced by i.c.v. infusion of AβOs in mice.

Methods:

Three month‐old male Swiss mice were pre‐treated with AZ formulation (Instanth NEO, Prodiet Medical Nutrition) or an isocaloric placebo diet for 4 weeks orally by gavage. After treatment, the animals received an infusion of 10 pmol AβOs (or equivalent vehicle volume) via i.c.v. in a final volume of 3 microliters and were assessed in cognitive tasks. Ten days after AβOs infusion, the animals were anesthetized and the brains were removed, fixed with 4% paraformaldehyde and cryoprotected in sucrose. To determine if the AZ formulation prevents microglial activation, frozen 40 micrometer coronal brain sections were obtained on a cryostat (Leica Microsystems) and stored in phosphate‐buffered saline, 0.05% sodium azide at 4°C. Free‐floating immunohistochemistry was performed with groups of 4–5 hippocampal sections per animal. After 2 hours blocking step (0,15% Triton X‐100; 5% BSA), the sections were incubated overnight with anti‐Iba1 primary antibody (1:400; Wako), washed and incubated for 2 h with an Alexa Fluor 488‐conjugated secondary antibody (1:1000; Life Technologies) and mounted with ProLong Gold Antifade Mountant with DAPI. Images were acquired on a ZEISS microscope. Four experimental groups with 5 animals per group were used, 2 groups with control formulation and 2 groups with AZ formulation.

Results:

Pre‐treatment with the AZ formulation prevented microglial activation induced by AβOs in mice (Fig. 1).

Conclusion:

These results suggest a possible mechanism by which the AZ formulation prevents cognitive damage in this mouse model of AD.

Financial Support: grant supported by Prodiet Medical Nutrition

A ‐ Representative image of microglial cels labeled with Iba‐1 in CA1 hippocampal sections from 3 month‐old male mice 10 days after i.c.v. infusion of AβOs (scale bar = 50um). B‐D – Quantification of integrated fluorescence density of Iba‐1 labeling in CA1 hippocampal region (B), Iba‐1 positive area (C), and total Iba‐1+ cells (D). Bars represent means ± SEM; n = 5 mice per experimental group (4‐5 CA1 images per animal).

 

*Research team: 

Luciana Siqueira, M.Sc.1; Hellin dos Santos, M.Sc.2; Ana Paula Celes3; Sergio Ferreira, PhD4.

1Institute of Biomedical Science, Federal University of Rio de Janeiro, Rio de Janeiro, Rio de Janeiro; 2Prodiet Medical Nutrition, curitiba, Parana; 3Prodiet Medical Nutrition, Rio de Janeiro, Rio de Janeiro; 4Institute of Biophysics Carlos Chagas Filho & Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, Rio de Janeiro, Rio de Janeiro.

 

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