Evidence map›Paper›PMID 40570189›Full record

ReviewThe Biochemical journal2025

Role of LRRK2 in axonal transport and Parkinson's disease.

Björn Twellsieck, C Alexander Boecker

Abstract readReview
In one paragraph

Review in The Biochemical journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Lysosomal homeostasis at the crossroads of neurodegeneration.The Journal of clinical investigation · 2026
    Review
  6. Review
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

2 authors.

Björn TwellsieckDepartment of Neurology, University Medical Center Goettingen, 37077 Goettingen, Germany.ORCID 0009-0004-5131-8796
C Alexander BoeckerDepartment of Neurology, University Medical Center Goettingen, 37077 Goettingen, Germany.ORCID 0000-0001-9701-5273

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Axonal transport is crucial for neuronal health and function, facilitating the delivery of newly synthesized material from the soma via anterograde transport and the removal of aged proteins and damaged organelles for degradation via retrograde transport. Emerging evidence links Parkinson's disease (PD)-causing mutations in the leucine-rich repeat kinase 2 (LRRK2) gene to dysfunctional axonal transport. Pathogenic LRRK2 mutations induce increased LRRK2 kinase activity, leading to the hyperphosphorylation of RAB proteins, which are key regulators of intracellular trafficking and transport. Here, we review the current literature on how LRRK2 affects the axonal transport of different cargoes, focusing on synaptic vesicle precursors, mitochondria, and autophagosomes. We further discuss how LRRK2 influences cytoskeletal dynamics and how it affects vesicle trafficking at the Golgi, which may indirectly contribute to its effect on axonal transport. This review summarizes our current understanding of how pathogenic LRRK2 hyperactivation disrupts axonal transport and how this may be linked to the neurodegeneration of PD.

Indexed as

Axonal TransportLeucine-Rich Repeat Serine-Threonine Protein Kinase-2Parkinson DiseaseAnimalsHumansMitochondriaMutationSynaptic VesiclesLeucine-Rich Repeat Serine-Threonine Protein Kinase-2LRRK2 protein, humanaxonal transportLRRK2Parkinson’s diseaseRAB GTPases

Identifiers

PMID40570189
PMCPMC12312394

What OpenQuestion holds

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Registered trials

None linked

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.