ArticleActa neuropathologica2026
Ser423-phosphorylated MECP2 (MECP2-pS423) accumulates in human brain, cerebrospinal fluid and serum in sporadic Alzheimer's disease.
Article in Acta neuropathologica, 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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Abstract
Methyl-CpG-binding protein 2 (MECP2) is a nuclear protein that serves as a global epigenetic repressor. Activity-dependent Ser421-phosphorylation is permissive to translocation of mouse Mecp2 to the cytoplasm, thereby reducing the repressor functions and activating neurotrophins. Mecp2-pS421 levels increase in neuron soma of AD (APP/PS1) mouse model and ablating Mecp2 increases activity of glycogen synthase kinase 3 beta, implying a link between MECP2 phosphorylation and Tau pathology in Alzheimer's disease (AD). It is currently unknown whether phosphorylation at the corresponding site of human MECP2-pS423 plays a role in AD. We developed an MECP2-pS423-specific antibody, and a quantitative selective reaction monitoring (SRM) assay based on LC-MS/MS analysis, and we used immunohistochemistry and proteomics to study MECP2-pS423 in human brain, cerebrospinal fluid (CSF), and serum specimens. In postmortem cortex and hippocampus, MECP2-pS423 expression increased across the clinicopathological spectrum of AD and correlated with histological progression and cognitive deficits. At the cellular level, MECP2-pS423 and pTau colocalized in granulovacuolar degeneration (GVD) bodies and neuritic plaques. Phosphoprotein levels of MECP2-pS423 increased in CSF and serum samples from patients clinically diagnosed as having AD premortem. Moreover, we found that a primate-specific and N-terminus truncated MECP2-E3 isoform mRNA was increased in postmortem middle temporal gyrus (MTG) of patients with AD. The results suggest that MECP2-pS423 is a promising mechanism-based biomarker and potential therapeutic target because its accumulations correlate with pathological and cognitive deficit in brain, CSF, and serum of human sporadic AD.
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