AI Article Synopsis
- * Recent studies link the disruption of palmitoylation to neurodegenerative diseases, impacting proteins like amyloid precursor protein, BACE1, and others involved in neuronal dysfunction.
- * The review discusses new findings on palmitoylation's role in neurodegeneration and investigates potential treatments that could target this process.
Article Abstract
Palmitoylation, a lipid-based posttranslational protein modification, plays a crucial role in regulating various aspects of neuronal function through altering protein membrane-targeting, stabilities, and protein-protein interaction profiles. Disruption of palmitoylation has recently garnered attention as disease mechanism in neurodegeneration. Many proteins implicated in neurodegenerative diseases and associated neuronal dysfunction, including but not limited to amyloid precursor protein, β-secretase (BACE1), postsynaptic density protein 95, Fyn, synaptotagmin-11, mutant huntingtin, and mutant superoxide dismutase 1, undergo palmitoylation, and recent evidence suggests that altered palmitoylation contributes to the pathological characteristics of these proteins and associated disruption of cellular processes. In addition, dysfunction of enzymes that catalyze palmitoylation and depalmitoylation has been connected to the development of neurological disorders. This review highlights some of the latest advances in our understanding of palmitoylation regulation in neurodegenerative diseases and explores potential therapeutic implications.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11450541 | PMC |
| http://dx.doi.org/10.1523/JNEUROSCI.1225-24.2024 | DOI Listing |
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