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Plasma proteomics identify biomarkers predicting Parkinson’s disease up to 7 years before symptom onset.

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Excellent, the earlier it can be found and treated the better.

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Our machine-learning model accurately identifies all Parkinson patients and classifies 79% of the pre-motor individuals up to 7 years before motor onset by analysing the expression of eight proteins—Granulin precursor, Mannan-binding-lectin-serine-peptidase-2, Endoplasmatic-reticulum-chaperone-BiP, Prostaglaindin-H2-D-isomaerase, Interceullular-adhesion-molecule-1, Complement C3, Dickkopf-WNT-signalling pathway-inhibitor-3, and Plasma-protease-C1-inhibitor.

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What most of those have in common is they are anti-inflammatory and increase in response to a high inflammatory state.

There are two exceptions. Complement C3 which leads to an increase in Complement C5a. C5a is on the regulator list as downregulated. C5a upregulates NF-kb, ROS, TNF-α, IL-8, IL-1β, CCL5 (RANTES) and other inflammatory cytokines. The other one is ICAM-1 also on the regulator list as downregulated. ICAM-1 is upregulated by inflammatory cytokines and directs cytokines to the site of injury.

What all have in common is a reaction to an inflammatory state.

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Parkinson’s disease (PD) is a complex and increasingly prevalent neurodegenerative disease of the central nervous system (CNS). It is clinically characterised by progressive motor and non-motor symptoms that are caused by α-synuclein aggregation predominantly in dopaminergic cells, which leads to Lewy body (LB) formation
Plasma proteomics identify biomarkers predicting Parkinson’s disease up to 7 years before symptom onset

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Here, we show that αSyn induces cofilin pathology in hippocampal neurons via a cellular PrPC-CCR5 dependent pathway. Moreover, cofilin dysregulation mediates dendritic spine impairment in response to αSyn, which is rescued by CCR5 inhibition. Based on the present data, we propose a novel action of CCR5 to exert allosteric regulation of the αSyn-activated neuronal PrPC/NOX complex that elicits a pathological cofilin rod response resulting in spine disruption. Antagonists of CCR5 may therefore protect synapses to provide treatment for cognitive impairment in LBD (Lewy Body Dementia). α-Synuclein triggers cofilin pathology and dendritic spine impairment via a PrPC-CCR5 dependent pathway

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I think it's self evident and don't have to say anything about leronlimab's effect.