Durk Pearson & Sandy Shaw’s®
Life Extension NewsTM
Volume 15 No. 4 • August 2012


Recent Results Highlight Importance of BDNF in
Maintaining Youthful Cognitive Abilities

In a recent paper,1 researchers report that the age-dependent deficits in long-term synaptic plasticity and loss of dendritic spines in the hippocampus of aged Fisher 344 rats were closely associated with reduced histone acetylation. Histones are proteins surrounding DNA that, by various chemical modifications, such as acetylation, determine whether genes are available for expression or are prevented from being expressed. In this paper,1 the aging deficits were linked to upregulation of HDAC2, a particular histone deacetylase, and decreased expression of a histone acetyltransferase. The researchers found that a key gene, BDNF, was affected by these changes and that these cognitive deficits could be rescued by enhancing BDNF and TrkB (BDNF receptor) expression via HDAC inhibition or by directly activating trkB receptors.

The authors suggest that “epigenetic or pharmacological enhancement of BDNF-trkB signaling could be a promising strategy for reversing cognitive aging.”

Reference

  1. Zeng et al. Epigenetic enhancement of BDNF signaling rescues synaptic plasticity in aging. J Neurosci 31(49):17800-10 (2011).

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