Reducing HuD Levels Alleviates Alzheimer's Disease Pathology in 5xFAD Mice.

Abstract

Alzheimer's disease (AD) is the most common neurodegenerative pathology in older persons. The accumulation of amyloid β (Aβ) plaques is a major contributor to AD development. The RNA-binding protein HuD/ELAVL4 has been implicated in the formation of Aβ plaques, but its role in AD is unclear. Here, we report that ablation of HuD from CAMK2Aneurons (HuDcKO) in the 5xFAD mouse model of AD results in a significant reduction of Aβ plaques and the alleviation of some AD-associated behaviors. Given the lack of effective therapies for AD, we propose that reducing HuD levels or function can contribute to diminishing Aβ plaque formation and AD-associated pathology.