ArticleActa neuropathologica2026
Deletion or immunotherapeutic blockade of FcγRIIb (CD32b) impairs α-Syn propagation in vivo.
Article in Acta neuropathologica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD), the most prevalent neurodegenerative movement disorder, is characterised by widespread alpha-synuclein (α-Syn) pathology in the brain and the progressive degeneration of nigrostriatal dopaminergic neurons. Experimental and clinicopathological data support a templated, prion-like component to α-Syn spread; however, the cellular mechanisms governing fibril uptake and intercellular transmission remain incompletely defined. Fc gamma receptor IIb (FcγRIIb or CD32b), the sole cross-species inhibitory Fcγ receptor, has been implicated in α-Syn internalisation in vitro, though its contribution to α-Syn propagation in vivo is not well established. Here, we examine the role of FcγRIIb in α-Syn seeding, propagation, and neurotoxicity in vivo using the preformed fibril (PFF) α-Syn intracranial injection model in mice. Genetic ablation of murine FcγRII reduced phosphorylated α-Syn (pα-Syn) burden and anatomical distribution across multiple brain regions at 90 days post-PFF injection, consistent with impaired development of Lewy-like pathology. Attenuated pα-Syn pathology was accompanied by reduced microglial reactivity, preservation of nigrostriatal dopaminergic integrity, and protection from PFF-associated motor and exploratory deficits. In parallel, pharmacological blockade of human (h) FcγRIIb using monoclonal antibodies reduced acute-phase pα-Syn accumulation in hFcγRIIb-transgenic mice following PFF challenge. Collectively, these findings identify FcγRIIb as a critical regulator of α-Syn propagation in vivo and support receptor-targeted blockade as a mechanistically distinct and therapeutically tractable strategy for modifying disease progression in PD and related α-synucleinopathies.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.