Mitochondrial dysfunction and oxidative stress are consistent features of multiple neurodegenerative diseases including Alzheimer’s disease (AD).
Because strategies that promote acute neuroprotection have not successfully translated into clinical practice, studies to understand repair/recovery mechanisms that promote functional recovery have emerged.
The recurring failure to translate neuroprotective strategies in animal models into clinical settings prompted us to reevaluate existing preclinical stroke models.
Nucleic acid secondary structures, such as G-quadruplexes and i-motifs, are emerging as important regulators of gene expression in the nervous system.
This project focuses onhow phenotypes of neurons generated in the adult subventricular zone (SVZ) are specified and how these neurons integrate into matureolfactory bulb circuits.
Stroke-induced brain injury has been viewed mainly from a neurocentric perspective, with much attention given to the primary injury site and its penumbra.