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This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 34 out of 100. Disease mechanisms

Topic: Brain proteins, microglia and lab models

Plain-language summary

Alzheimer’s disease (AD) and related tauopathies such as frontotemporal dementia (FTD) or traumatic brain injury (TBI) are neurodegenerative disorders characterized by progressive loss of memory and cognitive function. The main histopathological features of AD are amyloid-β plaques and Tau neurofibrillary tangles, suggested to interfere with neuronal function and to cause microtubule (MT) destabilization. We recently demonstrated that low mechanical forces promote MT stabilization, which in turn promotes axon growth and neuronal maturation. As neurites may become dystrophic due to MT destabilization in tauopathies, we hypothesized that force-induced MT stabilization is neuroprotective in cell models subjected to tauopathy-like stress. We set up two different pathological cellular models subjecting them to AD-related Tau pathology stressors. We found that exposure of mouse primary neurons to Tau oligomers and neurons derived from human induced pluripotent stem cell (hiPSC) to amyloid-β oligomers resulted in neurotoxic effects such as axonal shortening, reduction in dendrite number, and MT destabilization. Mechanical stimulation (i) prevented delays in axonal extensions and dendrite sprouting, restoring axon outgrowth to physiological levels, and (ii) compensated for axonal MT destabilization by increasing MT stability to levels higher than in control conditions. In summary, we here demonstrate that low mechanical force can be used as a neuroprotective extrinsic factor to prevent MT destabilization and axon degeneration caused by AD-like or tauopathy-like stressors.

What this study adds

Evidence grade: Low

In cell models exposed to tau or amyloid-beta oligomers, mechanical stimulation prevented axon and dendrite loss and raised microtubule stability above normal levels. These are laboratory cell experiments, so it is too early to say whether this approach could help patients.

Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Galeotti, A. A., Santucci, L., Klimek, J., Kabbani, M. A. A., Zempel, H., & Raffa, V. (2025). Mechanical stimulation prevents impairment of axon growth and overcompensates microtubule destabilization in cellular models of Alzheimer’s disease and related Tau pathologies. Frontiers in Medicine. https://doi.org/10.3389/fmed.2025.1519628

Vancouver

Galeotti AA, Santucci L, Klimek J, Kabbani MAA, Zempel H, Raffa V. Mechanical stimulation prevents impairment of axon growth and overcompensates microtubule destabilization in cellular models of Alzheimer’s disease and related Tau pathologies. Frontiers in Medicine. 2025. doi:10.3389/fmed.2025.1519628. PMID: 40438379.

BibTeX

@article{galeotti2025-40438379,
  author  = {Galeotti, Alice Alessandra and Santucci, Lorenzo and Klimek, Jennifer and Kabbani, Mohamed Aghyad Al and Zempel, Hans and Raffa, Vittoria},
  title   = {{Mechanical stimulation prevents impairment of axon growth and overcompensates microtubule destabilization in cellular models of Alzheimer’s disease and related Tau pathologies}},
  journal = {Frontiers in Medicine},
  year    = {2025},
  doi     = {10.3389/fmed.2025.1519628},
  pmid    = {40438379},
  url     = {https://doi.org/10.3389/fmed.2025.1519628}
}

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.

Key findings

Why it matters

In cell models exposed to tau or amyloid-beta oligomers, mechanical stimulation prevented axon and dendrite loss and raised microtubule stability above normal levels. These are laboratory cell experiments, so it is too early to say whether this approach could help patients.

Study details

How this study scored 34/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 1 of 4; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 4 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomized / blinded 0 of 2; Times cited 1 of 7; Citations per year 0 of 5; Impact for its field and year 2 of 6; Cited by studies here 0 of 6; Still being cited 0 of 4; Senior author's track record 2 of 4; Institution's track record 1 of 3; Multicenter collaboration 1 of 3; Indexed in PubMed 2 of 2; Free to read 2 of 2. Total 34 of 100.34 of 100 points earned66 not earned

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (Frontiers in Medicine)
Journal's citation record 1 / 4 Frontiers in Medicine: journal h-index 149 (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 4 / 5 2025 — within 3 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 Not stated whether this was studied in people — scores zero (not stated in the record — scored 0)
Randomized / blinded 0 / 2 No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited 1 / 7 Cited 2 times (OpenAlex, 2026-10-10)
Citations per year 0 / 5 0.7 citations a year over 3 year(s) since 2025
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 0 / 4 Cited 2 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 2 / 4 Last-listed author Vittoria Raffa: h-index 38 (OpenAlex, whole career)
Institution's track record 1 / 3 University of Pisa: institution h-index 907 (OpenAlex)
Multicenter collaboration 1 / 3 OpenAlex lists 3 institution(s) in 2 countries
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 40438379)
Free to read 2 / 2 Free to read
Total 34 / 100 —

What each of these 20 components measures, and what this score is not →

Read the original

Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).

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