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Updated: Mar 13, 2026

Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits
Published on: March 16, 2016
REAC technology modifies pathological neuroinflammation and motor behaviour in an Alzheimer's disease mouse model
Luca Lorenzini1, Alessandro Giuliani2, Sandra Sivilia2
1IRET Foundation, Ozzano Emilia, Italy.
Abstract:
The search for new therapeutic approaches to Alzheimer disease (AD) is a major goal in medicine and society, also due to the impressive economic and social costs of this disease. In this scenario, biotechnologies play an important role. Here, it is demonstrated that the Radio Electric Asymmetric Conveyer (REAC), an innovative technology platform for neuro- and bio-modulation, used according to the neuro-regenerative protocol (RGN-N), significantly increases astroglial reaction around the amyloid plaques in an AD mouse model, as evaluated by GFAP-immunoreactivity, and reduces microglia-associated neuroinflammation markers, as evaluated by Iba1-immunoreactivity and mRNA expression level of inflammatory cytokines TREM. IL1beta, iNOS and MRC1 were not affected neither by the genotype or by REAC RGN-N treatment. Also observed was an increase in locomotion in treated animals. The study was performed in 24-month-old male Tg2576 mice and age-matching wild-type animals, tested for Y-maze, contextual fear conditioning and locomotion immediately after the end of a specific REAC treatment administered for 15 hours/day for 15 days. These results demonstrated that REAC RGN-N treatment modifies pathological neuroinflammation, and mitigates part of the complex motor behaviour alterations observed in very old Tg2576 mice.
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