Affiliations: [a] Department of Neurology Cerebral Vascular Disease Research Laboratories, Miami, FL, USA
| [b] Neuroscience Program, University of Miami Miller School of Medicine, Miami, FL, USA
| [c] Centro de Neurociencias, Instituto de Investigaciones Científicas y Servicios de Alta Tecnología (INDICASAT AIP), City of Knowledge, Panama, Republic of Panama
Correspondence:
[*]
Correspondence to: Miguel A. Perez-Pinzon, Department of Neurology, D4-5, University of Miami, Miller School of Medicine, P.O. Box 016960, Miami, FL 33101, USA. Tel.: +1 305 243 7698; Fax: +1 305 243 6955; E-mail: [email protected].
Abstract: Cerebral ischemia affects millions of people worldwide and survivors suffer from long-term functional and cognitive deficits. While stroke and cardiac arrest are typically considered when discussing ischemic brain injuries, there is much evidence that smaller ischemic insults underlie neurodegenerative diseases, including Alzheimer’s disease. The “regenerative” capacity of the brain relies on several aspects of plasticity that are crucial for normal functioning; less affected brain areas may take over function previously performed by irreversibly damaged tissue. To harness the endogenous plasticity mechanisms of the brain to provide recovery of cognitive function, we must first understand how these mechanisms are altered after damage, such as cerebral ischemia. In this review, we discuss the long-term cognitive changes that result after cerebral ischemia and how ischemia alters several plasticity processes. We conclude with a discussion of how current and prospective therapies may restore brain plasticity and allow for recovery of cognitive function, which may be applicable to several disorders that have a disruption of cognitive processing, including traumatic brain injury and Alzheimer’s disease.
