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Parkinson’s Disease Onset in Light of Acquired Irreversible Piezo2 Channelopathy
Sonkodi B.. Preprints.org, 2026-09-23
Topic: Disease mechanisms in lab and animal studies
Plain-language summary
Neurodegenerative diseases posit a global challenge due to their aging-dependent increasing incidence around the world. The three most prevalent one, namely Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis are multisystem, progressive and degenerative diseases with underlying environmental and genetic risk factors. Not a single common initiating cause had been attributed to these neurodegenerative diseases due to their multifactorial disease background. Acquired irreversible Piezo2 channelopathy was first proposed as such a primary microdamage in the case of ALS in 2022, and later in the case of Alzheimer’s disease. Even though it has been suggested in 2025 that the impairment of the ultrafast ultradian cerebellar-hippocampal axis may initiate Parkinson’s disease due to acquired irreversible Piezo2 channelopathy, but detailed mechanistic introduction has been at need. Therefore, the current manuscript meant to introduce how the Piezo2-containing cerebellar Purkinje cells and deep cerebellar nuclei, more specifically dentate nuclei, principally fine-modulates the dopamine release of the neurons of substantia nigra pars compacta, initiates an ultrafast intermittent control strategy of postural control, and initiates beta and cerebellar theta synchronization. Consequently, the acquired irreversible Piezo2 channelopathy of the cells of deep cerebellar nuclei may initiate Parkinson’s disease onset by terminally impairing the fine-regulation of dopamine release, the intermittent cerebellar control strategy, the ultrafast ultradian cerebellar-hippocampal axis in association with energy generation switch from OXPHOS during acute stress responses.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Sonkodi, B. (2026). Parkinson’s Disease Onset in Light of Acquired Irreversible Piezo2 Channelopathy. Preprints.org. https://doi.org/10.20944/preprints202609.1965.v1
Vancouver
Sonkodi B. Parkinson’s Disease Onset in Light of Acquired Irreversible Piezo2 Channelopathy. Preprints.org. 2026. doi:10.20944/preprints202609.1965.v1.
BibTeX
@article{sonkodi2026-22979f3e,
author = {Sonkodi, B.},
title = {{Parkinson’s Disease Onset in Light of Acquired Irreversible Piezo2 Channelopathy}},
journal = {Preprints.org},
year = {2026},
doi = {10.20944/preprints202609.1965.v1},
url = {https://doi.org/10.20944/preprints202609.1965.v1}
}
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Key findings
- Not a single common initiating cause had been attributed to these neurodegenerative diseases due to their multifactorial disease background.
- Acquired irreversible Piezo2 channelopathy was first proposed as such a primary microdamage in the case of ALS in 2022, and later in the case of Alzheimer’s disease.
- Even though it has been suggested in 2025 that the impairment of the ultrafast ultradian cerebellar-hippocampal axis may initiate Parkinson’s disease due to acquired irreversible Piezo2 channelopathy, but detailed mechanistic introduction has been at need.
- Therefore, the current manuscript meant to introduce how the Piezo2-containing cerebellar Purkinje cells and deep cerebellar nuclei, more specifically dentate nuclei, principally fine-modulates the dopamine release of the neurons of substantia nigra pars compacta, initiates an ultrafast intermittent control strategy of postural control, and initiates beta and cerebellar theta synchronization.
- Consequently, the acquired irreversible Piezo2 channelopathy of the cells of deep cerebellar nuclei may initiate Parkinson’s disease onset by terminally impairing the fine-regulation of dopamine release, the intermittent cerebellar control strategy, the ultrafast ultradian cerebellar-hippocampal axis in association with energy generation switch from OXPHOS during acute stress responses.
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Study details
- Evidence strengthLow
How this study scored 16/100
Preprint — not yet peer-reviewed. It scored 21 on the same rubric, but non-peer-reviewed sources are capped at 16, so it shows as 16. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it. We have no data on times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multicenter collaboration, so those were left out: it earned 13 of the 62 points we could judge it on, which is 21 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 2 / 10 | Tier 4 — not a peer-reviewed journal (Preprints.org) |
| Journal's citation record | 0 / 4 | Not a journal article, so the journal's record does not count |
| 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 | 4 / 10 | Preprint — not yet peer-reviewed. Hosted on a preprint server. |
| How recent | 5 / 5 | 2026 — within 1 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 | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multicenter collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 1 / 2 | Not in PubMed, but has a DOI |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 13 / 62 | Scored on 12 of 20 parts. We have no data for the rest, so they are left out: 13 of the 62 points we could judge it on is 21 out of 100. |
| Total | 21 / 100 | Capped to 16 because this is not a peer-reviewed article. |
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