New Advances in Brain Remodeling and Recovery in Cerebrovascular Diseases

Dear Colleagues,

Old age is associated with an enhanced susceptibility to neurodegenerative diseases. Despite the initial hope that cell-based therapies may stimulate restorative processes in the degenerative brain, it is now recognized that the aging processes may promote an unfavorable environment for such treatments. Alternatively, in the last several years, many groups have focused on exploiting brain plasticity, that is preserved to some extent even in the old brains, to enhance endogenous repair mechanisms of the brain after insults, such as traumatic brain injury or cerebral ischemia. Virtually all drug interventions that have been successful preclinically in animal models have failed to translate this success to the clinical setting. The failure to consider aging, brain plasticity, and complexity and heterogeneity of human diseases and co-morbidities may render neuroprotective drugs less efficacious in clinical practice. Brain plasticity allows continuous remodeling of brain structure and function during aging and disease. People who incur a brain injury are prone to the development of neurodegenerative and neuroendocrine disorders. Thus, a traumatic brain injury (TBI) can trigger pathological changes within brain circuits and might lead to long-term cognitive and neuropsychological impairments. However, our understanding of secondary injury mechanisms is limited. Astrocytes play an important role in brain repair after brain injury and astrocyte-mediated mechanisms are likely important in injury-induced synapse remodeling. Old age is associated with an enhanced susceptibility to stroke, and aged animals recover poorly from brain injuries as compared to young rodents. Despite the initial hope that cell-based therapies may stimulate restorative processes in the ischemic brain, it is now recognized that aging processes may promote an unfavorable environment for such treatments. It is also well established that overt brain lesions, such as strokes, initiate vigorous neurogenesis in the subventricular zone of adult and even aged animals. However, it seems that most of the newly generated neurons in the subventricular zone either will die or never reach the infarcted area. It could be shown that the aged rat brain is not refractory to cell-based therapy as previously thought, and that it also supports plasticity and remodeling. Similarly, contrary to prevailing dogma, astrocytic scar formation is not a principal cause for the failure of injured mature CNS axons to regrow across severe CNS lesions and that scar-forming astrocytes permit and support robust amounts of appropriately stimulated CNS axon regeneration. This Special Issue of Biomedicines, will provide up-to-date information on molecular, cellular, and behavioral events associated with brain remodelling in response to aging and disease and open new avenues for treatment options.

Prof. Dr. Aurel Popa-Wagner
Guest Editor

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• aging
• stroke
• traumatic brain injury
• epilepsy
• Alzheimer’s disease
• schizophrenia
• depression