ELAV proteins and neurodegeneration: which role in Alzheimer's desease?

• Autorzy: Amadio M.
• Języki publikacji: EN

Abstrakty

EN

Increasing evidence highlights loss of RNA homeostasis as a central feature of many pathological states, including neurodegenerative diseases. The post‑transcriptional control of gene expression and its role in neurodegenerative pathologies are gaining increasing attention. Among RNA‑binding factors, ELAV proteins are master regulators of many cellular functions by influencing the RNA metabolism (from splicing to translation) of genes with crucial roles in various physio‑pathological contexts. Several ELAV‑target transcripts are linked to synaptic plasticity, stress response, survival, and proliferation. Evidence from our and other laboratories showed that neuronal ELAV (nELAV) members control gene expression in memory formation, and their alteration may contribute to cognitive impairment associated with Alzheimer’s disease (AD). We found that the content of nELAV proteins is significantly decreased along with clinical dementia progression in the hippocampi of AD brains, where it inversely correlates with the amount of amyloid‑β (Aβ). In turn, ELAV can affect Aβ precursor protein (APP) processing. The contribution of ELAV members to the neuronal homeostasis and their alteration in neurodegeneration (such as in AD) will be discussed in light of a wider, more complex proscenium where the post‑transcriptional (f)actors (e.g. different RBPs, coding and non-coding RNAs) play their role determining the fate of a given transcript.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2019
• Tom: 79
• Numer: Suppl.1
• Opis fizyczny: p.XXXI

Twórcy

autor

Amadio M.

• University of Pavia, Pavia, Italy