I would need to read up on this to say anything of any use. I am too busy at the moment to do this.
Parkinson’s disease (PD) is a neurodegenerative disorder with both genetic and environmental factors contributing to pathogenesis. Viral infections are potential environmental triggers that influence PD pathology. Using ViroFind, an unbiased platform for whole virome sequencing, along with quantitative PCR (qPCR), we identified human pegivirus (HPgV) in 5 of 10 (50%) of PD brains, confirmed by IHC in 2 of 2 cases, suggesting an association with PD. All 14 age- and sex-matched controls were HPgV negative. HPgV-brain positive patients with PD showed increased neuropathology by Braak stage and Complexin-2 levels, while those positive in the blood had higher IGF-1 and lower pS65-ubiquitin, supporting disruption in metabolism or mitophagy in response to HPgV. RNA-Seq revealed altered immune signaling in HPgV-infected PD samples, including consistent suppression of IL-4 signaling in both the brain and blood. Longitudinal analysis of blood samples showed a genotype-dependent viral response, with HPgV titers correlating directly with IL-4 signaling in a LRRK2 genotype–dependent manner. YWHAB was a key hub gene in the LRRK2 genotypic response, which exhibited an altered relationship with immune-related factors, including NFKB1, ITPR2, and LRRK2 itself, in patients with PD who are positive for HPgV. These results suggest a role for HPgV in shaping PD pathology and highlight the complex interplay between viral infection, immunity, and neuropathogenesis.
Press: Groundbreaking study finds possible virus link to Parkinson’s Disease
His team discovered the presence of Human Pegivirus — a virus not previously linked to any known disease — in half of the Parkinson’s patients studied.
“This is a blood-borne virus that can be found in 5-to-10% of healthy blood donors. It’s related to hepatitis C — and we found it in 50% of brains of patients with Parkinson’s disease.”
Because the virus is similar to hepatitis C, researchers now plan to investigate whether existing hepatitis C medications might also help treat or even prevent Parkinson’s.
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There is a correlation with a lot of chronic diseases and pathogens, especially with neurodegenerative disease.
This is why laboratory rodents live longer than wild, lack of predators (including pathogens).
This is why if humans were living an environment free of major pathogens and toxins (except for controlled bioflora) assuming good diet, exercise, sleep and lack of major stressors, they would live much longer IMO.
We already have evidence of that with hygiene, proper nutrition, clean water, vaccinations almost tripled the life span in the past 150 years… mainly by reducing premature deaths.
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I performed a search of the site and did not see this study posted. If it had been, I apologize. I make a special effort to find French papers on PD. Obviously this is in women. Note however, again, it does matter which specific statin is used, here even a broad class effect of lipophilic vs hydrophilic. Rather counter to previous hypothesis, it’s the lipophilic that had a positive effect. Given how long symptomless period for PD can be prior to diagnosis, I wonder if 5 years is enough.
Statin Use and Incidence of Parkinson’s Disease in Women from the French E3N Cohort Study
Yes, lipophilic looks better in this paper but overall association studies are mixed:
High LDL is protective in PD (per MR), so this might just be reverse causation (high LDL => statin use & lower PD risk):
- Protective role of apolipoprotein A and B in Parkinson’s disease: A prospective study from UK Biobank 2025: “Elevated baseline levels of serum ApoA (HR = 0.84, 95 % CI: 0.71–0.99, P = 0.047) and ApoB (HR = 0.67, 95 % CI: 0.57–0.78, P = 3.18E-07) were associated with a reduced risk of incident PD.”
- Association of cholesterol and glycemic state biomarkers with phenotypic variation and Parkinson’s disease progression: The Oxford Discovery cohort 2025: “HDL-C and total cholesterol differed across baseline PD phenotype clusters, with reduced levels associated with the most severe motor and non-motor phenotypes (psychological well-being, cognitive impairment, REM sleep behavior disorder, and daytime sleepiness). Higher HDL-C and total cholesterol, although the latter was attenuated after adjustment for statin use, were associated with better baseline activities of daily living (e.g., UPDRS-II score with 1 SD increase in HDL-C −0.74, 95%CI −1.22 to −0.26, p = 0.002) and non-motor features. Neither predicted the rate of motor or non-motor progression.”
Two RCTs tried lipophilic statins in early PD:
- Simvastatin: worsening motor symptoms in the simvastatin-treated group.
- Lovastatin: no significant difference in motor scores but possible beneficial effect in terms of dopaminergic cell loss.
Confirmed by MR: Causal relationship between PCSK9 inhibitor and common neurodegenerative diseases: A drug target Mendelian randomization study 2024: “HMGCR inhibitors increased the risk of PD (OR [95%] = 1.907 [1.502 to 2.312], p = 0.001)”
Not PD but see also: Mendelian Randomization Study of PCSK9 and HMG-CoA Reductase Inhibition and Cognitive Function 2022: “Using a wide range of cognitive function and dementia endpoints, we failed to find genetic evidence of an adverse PCSK9-related impact, suggesting a neutral cognitive profile. In contrast, we observed adverse neurocognitive effects related to HMGCR inhibition, which may well be outweighed by the cardiovascular benefits of statin use, but nonetheless may warrant pharmacovigilance.”
Gut disruption of GLP-1 might be the mechanism of action: Cardiovascular Health - #993 by adssx
Association studies + MR + RCT + Mechanistic understanding all point towards statins (and lipid-lowering in general?) being bad in PD.