Evidence map›Paper›PMID 41992320›Full record

ArticleJournal of neuroinflammation2026

Therapeutic targeting of blood-derived protein infiltration to modulate neuroinflammation in cerebellar ataxia.

Se Min Park, Seong Soon Kim, Eunji Cho, Gi Beom Lee, Ji Min Lee, Dong Woon Kim, Jong-Heon Kim, Jung-Eun Kim, Gee Euhn Choi, Ho-Won Lee and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroinflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Se Min Park *School of Life Science and Biotechnology, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, 41566, Republic of Korea.
Seong Soon Kim *Bio and Drug Discovery Division, Korea Research Institute of Chemical Technology, Daejeon, 34114, Republic of Korea.
Eunji Cho *Neurodegenerative Diseases Research Group, Korea Brain Research Institute, Daegu, 41062, Republic of Korea.
Gi Beom LeeSchool of Life Science and Biotechnology, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, 41566, Republic of Korea.
Ji Min LeeSchool of Life Science and Biotechnology, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, 41566, Republic of Korea.
Dong Woon KimDepartment of Oral Anatomy and Developmental Biology, College of Dentistry, Kyung Hee University, Seoul, 05505, Republic of Korea.
Jong-Heon KimBrain Science and Engineering Institute, Kyungpook National University, Daegu, 41404, Republic of Korea.
Jung-Eun KimDepartment of Neurology, Kyungpook National University Chilgok Hospital, Daegu, 41404, Republic of Korea.
Gee Euhn ChoiLaboratory of Veterinary Biochemistry, College of Veterinary Medicine, Jeju National University, Jeju, 63243, Korea.
Ho-Won LeeBrain Science and Engineering Institute, Kyungpook National University, Daegu, 41404, Republic of Korea.
Kyoungho SukBrain Science and Engineering Institute, Kyungpook National University, Daegu, 41404, Republic of Korea.
Jong Hyuk YoonNeurodegenerative Diseases Research Group, Korea Brain Research Institute, Daegu, 41062, Republic of Korea. jhyoon@kbri.re.kr.
Sehwan KimSchool of Life Science and Biotechnology, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, 41566, Republic of Korea. arputa@naver.com.
Sang Ryong KimSchool of Life Science and Biotechnology, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, 41566, Republic of Korea. srk75@knu.ac.kr.

Funding

Korea Healthcare Technology R&D HI21C1795Ministry of Science and ICT, South Korea 24-BR-02-03National Research Foundation of Korea RS-2022-NR075084National Research Foundation of Korea RS-2024-00408736
6 · The paper itself

Abstract

Neuroinflammation is one of the key drivers of spinocerebellar ataxia type 2 (SCA2), yet the role of prothrombin-derived proteins in its pathogenesis remains unclear. Here, we show that prothrombin-derived proteins, thrombin and prothrombin kringle-2 (pKr-2), are elevated in the plasma of patients with cerebellar ataxia (CA) and in the cerebellum of SCA2 mice. Intervention strategies, reinforcing the blood–brain barrier (BBB) with caffeine administration and inhibiting thrombin/pKr-2 production through oral administration of rivaroxaban, attenuated cerebellar infiltration of prothrombin-derived proteins, neuroinflammation, and motor deficits in SCA2 mice, whereas pKr-2 upregulation exacerbated neuronal damage and behavioral impairments. These findings reveal a distinct peripheral proteomic signature linked to a cerebellar pathogenic pathway and suggest that limiting the entry of prothrombin-derived proteins into the cerebellum may represent a critical therapeutic approach in CA.

Indexed as

Cerebellar AtaxiaNeuroinflammatory DiseasesProthrombinThrombinAnimalsBlood-Brain BarrierCerebellumHumansMaleMiceMice, TransgenicProthrombinThrombinBlood–brain barrierNeurodegenerationNeuroinflammationProthrombin-derived proteinsProthrombin kringle-2Spinocerebellar ataxia type 2

Identifiers

PMID41992320
PMCPMC13214360

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Registered trials

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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.