Cytoplasmic HDAC4 recovers synaptic function in the 3×Tg mouse model of Alzheimer's disease.

ABSTRACT:

Aims

Early dysfunction in Alzheimer's disease (AD) is characterised by alterations of synapse structure and function leading to dysmorphic neurites, decreased spine density, impaired synaptic plasticity and cognitive deficits. The class II member HDAC4, which recently emerged as a crucial factor in shaping synaptic plasticity and memory, was found to be altered in AD. We investigated how the modulation of HDAC4 may contribute to counteracting AD pathogenesis.

Methods

Using a cytoplasmic HDAC4 mutant (HDAC4^SD ), we studied the recovery of synaptic function in hippocampal tissue and primary neurons from the triple-transgenic mouse model of AD (3×Tg-AD).

Results

Here, we report that in wild-type mice, HDAC4 is localised at synapses and interacts with postsynap

SUBMITTER: Colussi C 

PROVIDER: S-EPMC10099707 | biostudies-literature | 2023 Feb

REPOSITORIES: biostudies-literature