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Article

Phenotype Differences Between ATP13A2 Heterozygous and Knockout Mice Across Aging.

International journal of molecular sciences - 22 Jul 2025

Croucher Kristina, Lepp Josephine K, Bechtold Jennifer, Hamad Edward J, Scott Sophia, Bittner Christian, Rogers Sara, Ong Christian, Boehme Shannon, Wang Zhuo, Lin Li, Wang Xinwen, Fleming Sheila M

Abstract excerpt

ATP13A2 is a lysosomal polyamine transporter with loss of function mutations linked to multiple neurodegenerative disorders including Parkinson's disease (PD). Knockout of ATP13A2 in mice leads to age-related sensorimotor impairments and in the brain lipofuscinosis, gliosis, and modest alpha-synuclein (αSyn) pathology. However, few studies have included ATP13A2 heterozygous mice as a comparison. In the present...

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Identifiers

PMID: 40806164
DOI: 10.3390/ijms26157030
PMCID: PMC12346011

Genes

ATP13A2
GFAP

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

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Phenotype Differences Between ATP13A2 Heterozygous and Knockout Mice Across Aging.PMID 40806164Read ↗

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Adult-Onset Deletion of <i>ATP13A2</i> in Mice Induces Progressive Nigrostriatal Pathway Dopaminergic Degeneration and Lysosomal AbnormalitiesSemantic proximity Read ↗

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α-Synuclein-Independent Histopathological and Motor Deficits in Mice Lacking the Endolysosomal Parkinsonism Protein Atp13a2Semantic proximity Read ↗

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ATP13A2 Loss of Function-Driven Polyamine Dysregulation Induces SAM Depletion and Epigenetic Astrocyte ToxicitySemantic proximity Read ↗

Spermidine suppresses glial inflammation and parkinsonian abnormalities in ATP13A2 deficiencySemantic proximity Read ↗

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