I will leave this up, because it’s already been on record, but it has been brought to my attention by @adssx that the among the people involved in this study there is at least one prominent fraudster.
CAUTION - DISREPUTABLE AUTHORS INVOLVED!!!
Longevity factor klotho and resistance to cognitive deficits in individuals with Parkinson’s disease and in an α-synuclein mouse model
https://www.jneurosci.org/content/early/2026/03/30/JNEUROSCI.1904-25.2026
Hmm. What do you think, @adssx? AD and not PD, but the alpha-synuclein here is very interesting in the context of PD. I wonder what this means.
Sex-Specific Associations of α-Synuclein Pathology With Tau Accumulation
https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2845874
Doesn’t look actionable to me?
Abstract only but serious team at UCSF.
If you have some free time, this is an interesting listen. An important methodological approach - why we need to question “established standards of care” (first 14 minutes are fluff, start at 14:30).
From Doubt to Discovery: The Fight to Redefine Parkinson’s | With Dr. Jonathan Sackner-Bernstein (via Power & Impact)
Among 82,605 women, 603 developed PD and 13,022 used CCBs. Women who started non-DiCCBs had higher PD risk than never users (hazard ratio [HR] = 1.56; 95% confidence interval [95% CI] = 0.99–2.46; P-trend ≤ 0.02). Among non-DiCCBs, diltiazem was associated with PD (HR = 2.20 [95% CI = 1.19–4.04]). There were no significant associations for CCBs overall, amlodipine, and non-amlodipine DiCCBs. In analyses without a lag, amlodipine (HR = 1.45 [95% CI = 1.13–1.87]) and diltiazem (HR = 1.63 [95% CI = 1.02–2.60]) were associated with PD. Results are consistent with trajectories of CCBs prescriptions in PD patients and controls.
Overall, CCBs were not associated with PD but women who started using diltiazem had higher PD incidence in lagged analyses. Diltiazem and amlodipine were associated with PD in analyses without a lag. These findings are consistent with case reports of parkinsonism induced by specific CCBs and warrant further studies and surveillance.
The positive association of amlodipine and non-DiCCBs, especially diltiazem, with PD represents an original finding. Although there are differences in their ability to cross the brain–blood barrier,7 all CCBs, including amlodipine/diltiazem, can penetrate the brain, especially during chronic treatment.4-6 […] One interpretation of our findings is that amlodipine and diltiazem aggravated motor symptoms in women with pre-existing presynaptic dopaminergic denervation and accelerated the PD diagnosis. There was a difference in the relationship of amlodipine and non-DiCCBs (including diltiazem) with PD. Whereas the association with amlodipine was restricted to analyses without a lag (ie, for relatively recent exposures), the association for non-DiCCBs (including diltiazem) was stronger in analyses with a 5-year lag. One possible explanation could be that longer exposure periods and higher cumulative doses may be required for non-DiCCBs than amlodipine; however, this difference must be interpreted with caution, given the small number of exposed cases. We did not show any association for verapamil, but the small number of exposed cases makes it difficult to draw firm conclusions. These findings warrant replication in studies with longer lags in order to better examine the temporal relation between exposure to non-DiCCBs and PD. If replicated, it remains to be demonstrated whether CCBs discontinuation in PD patients could, in some cases, improve symptoms.
In conclusion, our study found no evidence in favor of a neuroprotective role of CCBs for PD. Conversely, one possible explanation for our findings for amlodipine and non-DiCCBs (notably diltiazem) is that these drugs may accelerate the development of PD in patients with pre-existing presynaptic dopaminergic denervation.
Recent literature review:
12-week probiotic supplement containing nine bacterial strains (Bifidobacterium bifidum W23, Bifidobacterium lactis W51 and W52, Lactobacillus acidophilus W37, Levilactobacillus brevis W63, Lacticaseibacillus casei W56, Ligilactobacillus salivarius W24, and Lactococcus lactis W19 and W58) on anxiety symptoms in 61 individuals with PD and clinically significant anxiety. Both the probiotic (n = 30) and placebo (n = 31) groups showed significant within-group improvements on the Parkinson Anxiety Scale, with no significant between-group differences. The probiotic group showed a statistically significant improvement on the Montreal Cognitive Assessment compared with placebo (adjusted mean difference of 1.1 points; 95% confidence interval: 0.04–2.1; p = 0.043). No treatment effects were seen on other secondary outcomes, including depression, constipation, or motor symptoms.
Blood-based biomarkers of ferroptosis in Parkinson’s disease 2026
At baseline, UPDRS III-Worst OFF was positively correlated with log-4-HNE (p = 0.007). PDQ-39 was negatively correlated with log-ferritin concentration (p = 2.38 10−4), selenium concentration (p = 0.033) and the rs7887981 in the ACSL4 gene (p = 0.033).
Our results strongly support an association between 4-HNE levels and the progression of motor disability in advanced PD. They also provide multiple lines of evidence favoring a role for ferroptosis in PD progression. Subject to further validation, they could therefore be used to select and stratify patients for future clinical trials.
We also found that higher selenium and log-ferritin levels were both associated with a better quality of life, as attested by a lower PDQ-39 total score (−0.118 ± 0.055; p = 0.033 and − 4.324 ± 1.167; p = 2.38 10−4; respectively). But after adjustment for multiple comparisons, only the association between log-ferritin and PDQ-39 stayed significant (adjusted p-value = 0.094 and 1.34*10−3; respectively).
In particular, we found that lower log-ferritin levels at baseline were associated with a poorer quality of life. These results suggest that alterations to iron metabolism influenced PD severity in our cohort. Ferritin is an essential protein for iron storage in the body, and it serves as a marker of inflammation. Our observations are consistent with the reported lower concentration of ferritin in the substantia nigra of PD patients than in that of healthy patients (Dexter et al., 1990; Connor et al., 1995). Interestingly, ferritin degradation by ferritinophagy has been shown to be instrumental in triggering or maintaining ferroptosis (Ajoolabady et al., 2021). In a context of ferroptosis, low ferritin concentration may lead to an increase in the labile iron pool, causing oxidative damage and resulting in lipid peroxidation and an increase in 4-HNE levels. However, low ferritin levels may also be linked to mild iron deficiency or to iron consumption/relocation by macrophages during inflammatory responses.
Our findings provide evidence that enteric inflammation is present at a moderate level in prodromal PD, not higher than in individuals with established PD, and without concurrent changes in intestinal permeability.
Blood mtDNA markers of mitochondrial subtype and early-onset Parkinson’s disease biology 2026
MtDNA damage markers, particularly deletion burden, capture mitochondrial dysfunction arising from both genetic and environmental influences and are detectable across early clinical stages of PD. While not serving as stand-alone diagnostic biomarkers, mtDNA measures provide complementary biological information within a multimodal framework and may support patient stratification based on mitochondrial involvement using a minimally invasive approach.
These findings suggest that preserved glymphatic function may be associated with prolonged prodromal stability in iRBD.
=> Could this be a possible protective factor?
Together, the results highlight a critical role of inherited DSB repair deficiencies in PD etiology and suggest potential avenues for personalized risk prediction and prevention.
The surprising science behind red-light therapy — and how it really works
Researchers have seen benefits in animal models of Parkinson’s last for weeks after treatment, and early human trials are under way, using optical fibres that put the light close to the diseased cells
RFC1-related disorders: A case series of 4-aminopyridine and acetyl-DL-leucine treatment 2026
Tanganil failed?
In this multicenter case series of 30 genetically confirmed RFC1-positive patients, we evaluated the real-world effects of 4-AP and ADLL, both administered on a named patient use basis. Only a minority of patients reported subjective clinical benefits, and objective improvements were restricted to gait and observed in a similarly small proportion.
GLP1R expression and parkinson’s disease and related disorders in GLP-1RA-treated type 2 diabetes 2026
These findings link a mechanism-anchored genetic proxy for higher systemic GLP1R expression to a lower risk of incident PDRD among GLP-1RA–treated adults with type 2 diabetes. Systemic GLP1R-mediated pathways may be relevant to interindividual differences in observed PDRD risk, and genetic instruments for GLP1R expression may inform hypotheses for future PDRD trial design.
@John_Hemming: a few interesting papers here for you, especially on ferritin levels and mtDNA.
Of note, one of the authors is French fraudster Sylvain E. Lesné: Sylvain Lesné - Wikipedia
This guy deserves the death penalty. We shouldn’t read articles he contributed to. People who agreed to associate their names with his aren’t trustworthy either.
Forgot that one, on ferritin as well: Macrophage ferritin heavy chain/α-synuclein regulatory axis modulates ferroptosis during kidney injury 2026
Macrophages, endowed with remarkable phenotypic plasticity, are essential for orchestrating injury responses and regulating iron homeostasis. Given the central role of ferritin heavy chain (FtH) as a molecular rheostat linking iron sequestration to redox-dependent signaling, we examined how myeloid FtH governs renal iron trafficking and ensuing oxidative stress pathways during acute kidney injury (AKI). Transcriptome analysis revealed coupling of FtH deficiency in monocytes and macrophages with activation of ferroptosis, a regulated cell death associated with iron accumulation. Moreover, myeloid FtH deletion worsened AKI, increasing leukocyte infiltration and iron deposition, together with ferroptosis-associated gene induction, oxidative stress, and lipid peroxidation. Notably, α-synuclein (SNCA), an iron-binding protein and the main pathological driver of Parkinson’s disease, was robustly induced both by FtH deficiency and following AKI. Mechanistic studies showed that monomeric SNCA exhibits ferrireductase activity, amplifying redox cycling and promoting ferroptotic cell death. Furthermore, SNCA expression was elevated in kidney pathologies characterized by leukocyte expansion in both mouse models and human cohorts, suggesting that inflammatory microenvironments promote SNCA accumulation and redox imbalance. These findings define a macrophage FtH/SNCA regulatory axis as a key driver of ferroptosis in AKI, implicating SNCA as a pathological nexus between iron dyshomeostasis and inflammatory kidney injury.
In summary, our study uncovers a mechanistic pathway linking FtH deficiency in macrophages to heightened kidney injury via a macrophage SNCA/FtH regulatory axis that governs ferroptosis signaling. Myeloid FtH deletion and consequent perturbation of iron homeostasis foster excessive iron accumulation, which in turn precipitates enhanced ferroptotic cell death in the kidney. Importantly, the elevated expression of SNCA in macrophages correlates with kidney disease models characterized by marked leukocyte aggregation and may explain, at least in part, the observed association between CKD and an increased risk of neurodegenerative disorders. These findings position the macrophage FtH/SNCA regulatory axis as a mechanistic fulcrum whereby perturbations in iron homeostasis drive inflammatory kidney pathology and may serve as a peripheral conduit for excess SNCA dissemination to the central nervous system, potentially contributing to synucleinopathy development.
Wow. I had no idea. Insane that such people are not drummed out of all science platforms. If you commit scientific fraud, and it is proven, that should be a ban for life from all science platforms.
There needs to be a central database of all these fraudsters. Anyone who lands in that database should be permanently banned so they don’t cause further harm and waste resources.
Banning is not enough. Fine + jail.
You have probably previously posted about this paper. But today is the first time I have read it. And I have added tributyrin to my stack mainly on the basis of this paper. I see little downside, and because I believe chronic inflammation is a major factor in health and life span, I like supplements that reduce it as measured by hsCRP.