Stroke is a devastating condition afflicting mostly the elderly for which no viable medication exists to improve neuro-rehabilitation. In particular, great clinical benefit may accrue from deciphering and targeting basic neurobiological mechanisms underlying post-stroke CNS recovery both in structural and functional terms.
Clinical trials aimed at improving functional recovery after stroke has uniformly failed. One reason for this may be that very little genetic information is available describing the post-stroke events. Recent advances in genomics and DNA array technology may lead to the discovery of new therapeutic targets by uncovering the mechanisms underlying brain repair and regeneration after stroke. Several such studies have employed these techniques with the aim of identifying new therapeutic targets for stroke treatment. Some of these studies revealed changes in transcriptional activity of a variety of genes related to stress response, inflammation, acute- and delayed cell death in young rats, while later studies revealed a pathway associated with brain defense and tissue repair in a young mouse model of stroke (Tseveleki et al.) or neurovascular unit development genes. Some other studies were concerned with the gene expression in the contralateral hemisphere, which suggested the presence of bilateral effects and/or differential regulation.
An important omission of these studies is that they did not include aged animals. The importance of animal age in the physiological response to stroke is emphasized by a recent study that identified an age-specific sprouting or regeneration transcriptome that differentially regulates the process of brain reorganization after brain infarct in young vs. aged animals.
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