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REAC technology modifies pathological neuroinflammation and motor behaviour in an Alzheimer's disease mouse model
Lorenzini L, Giuliani A, Sivilia S, Baldassarro, Fernandez M, Lotti Margotti M, Giardino L, Fontani V et al.. Scientific reports, 2016-10-24
Topic: Amyloid, tau and blood-test diagnosis
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.
Key findings
- 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.
- 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.
Why it matters
In 24-month-old Tg2576 Alzheimer's model mice, REAC RGN-N treatment increased astroglial reaction around amyloid plaques, reduced some microglia-associated neuroinflammation markers, and increased locomotion. This is animal research and does not establish any treatment, cure, or prevention for Alzheimer's disease in people.
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Study details
- Evidence strengthLow
How this study scored 38/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Scientific reports) |
| Journal's citation record | 3 / 4 | Scientific Reports: journal h-index 463 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2016 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Laboratory or animal study (title names “mouse”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 3 / 7 | Cited 25 times (OpenAlex, 2026-10-10) |
| Citations per year | 1 / 5 | 2.1 citations a year over 12 year(s) since 2016 |
| Impact for its field and year | 2 / 6 | Cited 1.1× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 1 / 4 | Cited 12 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Laura Calzà: h-index 53 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Bologna: institution h-index 989 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 27775040) |
| Free to read | 2 / 2 | Free to read |
| Total | 38 / 100 | — |
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Read the original
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
APA 7th
Lorenzini, L., Giuliani, A., Sivilia, S., Baldassarro, Fernandez, M., Lotti Margotti, M., et al. (2016). REAC technology modifies pathological neuroinflammation and motor behaviour in an Alzheimer's disease mouse model. Scientific reports. https://doi.org/10.1038/srep35719
Vancouver
Lorenzini L, Giuliani A, Sivilia S, Baldassarro, Fernandez M, Lotti Margotti M, et al. REAC technology modifies pathological neuroinflammation and motor behaviour in an Alzheimer's disease mouse model. Scientific reports. 2016. doi:10.1038/srep35719. PMID: 27775040.
BibTeX
@article{lorenzini2016-27775040,
author = {Lorenzini, L. and Giuliani, A. and Sivilia, S. and Baldassarro and Fernandez, M. and Lotti Margotti, M. and Giardino, L. and Fontani, V. and others},
title = {{REAC technology modifies pathological neuroinflammation and motor behaviour in an Alzheimer's disease mouse model}},
journal = {Scientific reports},
year = {2016},
doi = {10.1038/srep35719},
pmid = {27775040},
url = {https://doi.org/10.1038/srep35719}
}
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