Analysis demonstrates dysregulation of RBPs in tauopathies, indicating potential compensatory mechanisms in Alzheimer's disease.
mice, as well as in samples from patients with Alzheimer's disease (AD). This change in expression is evident at both mRNA and protein levels and, in some cases, is accompanied by alterations in their subcellular localization. Our results suggest that RBP dysregulation is a common mechanism in various tauopathies and may be related to impaired TAU functionality. Furthermore, the upregulation of RBPs may represent a compensatory mechanism in response to deficits in synaptic translation.
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Silva-Llanes et al. (2026) studied this question.
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