Abstract

Traumatic brain injury (TBI) causes neural circuit reorganization that can lead to functional recovery. However, the molecular mechanisms underlying this reorganization remain poorly understood. Here, we show that inhibition of histone deacetylase 2 (HDAC2) promotes functional recovery after TBI by enhancing brain-derived neurotrophic factor (BDNF) expression and subsequent neuronal rewiring.

Key Findings

• HDAC2 expression is upregulated after TBI, limiting BDNF expression
• Pharmacological or genetic inhibition of HDAC2 increases BDNF levels
• HDAC2 inhibition promotes corticospinal tract rewiring
• Treatment leads to significant functional recovery in motor tasks

Impact

This work identifies HDAC2 as a potential therapeutic target for promoting recovery after brain injury and provides mechanistic insights into epigenetic regulation of neural plasticity.

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