ReviewNPJ Parkinson's disease2026
Progress in modelling ATP13A2-linked neurodegeneration.
Review in NPJ Parkinson's disease, 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
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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
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Authors and funding
4 authors.
Funding
Abstract
ATP13A2 is a lysosomal P5-ATPase highly expressed in the central nervous system, regulating polyamine, metal cation, and calcium homeostasis. Loss-of-function mutations cause an autosomal recessive juvenile form of Parkinson's disease called Kufor-Rakeb syndrome and other neurodegenerative disorders. Since the first clinical discovery of the Kufor-Rakeb syndrome, numerous ATP13A2-related models have emerged, leading to significant advances in understanding the physiology and pathophysiology of this protein. This review summarizes ATP13A2 structure, function, pathology, and insights gained from cellular and animal models, highlighting their value for elucidating disease mechanisms and therapeutic development across species and experimental systems, relevant to neurodegeneration research broadly.
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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.