ReviewBiomolecules & biomedicine2026
LAPTM proteins in neurological disorders - Autophagy-lysosome dysfunction and therapeutic targets: A review.
Review in Biomolecules & biomedicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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Authors and funding
3 authors.
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Abstract
Lysosomal-associated protein transmembrane (LAPTM) family members-LAPTM4A, LAPTM4B, and LAPTM5-regulate lysosomal integrity, autophagy-lysosome flux, lipid homeostasis, and immune signaling, pathways increasingly implicated in neurological disease. This review synthesizes structure-function evidence for LAPTM proteins and examines how their dysregulation contributes to Alzheimer's and Parkinson's disease, ischemia-reperfusion injury, and gliomas. Based on a targeted narrative analysis of primary and translational studies, we highlight that LAPTM proteins influence lysosomal acidification and membrane stability, endolysosomal trafficking, and ceramide/ion handling, thereby shaping protein aggregate clearance, oxidative stress responses, and microglia/macrophage polarization. Preclinical data link LAPTM5 to stroke outcomes via stress-kinase and lysosomal pathways, while LAPTM4A and LAPTM4B associate with glioma progression, immune evasion, and therapy resistance. Overall, LAPTM proteins represent promising biomarkers and therapeutic targets, warranting cell-type-resolved validation and central nervous system (CNS)-optimized delivery strategies, including gene therapy, small-molecule/degrader approaches, and multi-omics-guided patient stratification.
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