- Chair of Vascular Neurology, Dementia and Ageing, University Hospital Essen, University of Duisburg—Essen, Essen, GermanyInterests: aging; cerebrovascular diseases; brain plasticity; gene expression.; therapiesSpecial Issues and Topics in IMR Press journals
How aging and stress affect neural plasticity and depression
Increasing evidence demonstrates that neuroplasticity, a fundamental mechanism of neuronal adaptation, is affected in cerebrovascular conditions that include traumatic brain injury and brain ischemia. Age-related changes in neural plasticity play a significant role in the onset and development of cerebrovascular diseases. Despite the initial hope that cell-based therapies might stimulate restorative processes in the degenerative brain, we now recognized that aging processes may promote an unfavorable environment for such treatments. Alternatively, in the last several years, many groups have focused on exploiting brain plasticity, which is preserved to some extent even in old brains, to enhance the brain’s endogenous repair mechanisms after insults such as traumatic brain injury or cerebral ischemia.
Virtually all drug interventions that have been successful in animal models have failed to translate successfully to the clinical setting. The failure to consider the aging-brain’s plasticity and complexity, and the heterogeneity of human diseases and co-morbidities, may have rendered neuroprotective drugs less effective in clinical practice.
The main opponent of brain plasticity in the aged brain is neuroinflammation. It is becoming evident that with increasing age, the brain’s subtle but continuous neuroinflammation can provide the basis for disorders such as cerebral small vessel disease (cSVD) and consequent dementia. Moreover, advanced aging and a number of highly prevalent risk factors such as obesity hypertension, diabetes, and atherosclerosis, are increasingly understood to act as “silent contributors” to neuroinflammation—not only establishing the condition as a central pathophysiological mechanism, but also constantly fueling it. Acute neuroinflammation, often in the context of traumatic or ischemic CNS lesions, aggravates the acute damage and can lead to a number of pathological illnesses, such as depression, post-stroke dementia, and potentially, neurodegeneration. All of those sequelae impair recovery, and most of them provide the basis for further cerebrovascular events; thus, a vicious cycle develops. Recent advances in signaling pathways can potentially protect cells as well as provide treatment options for the maintenance of brain capillaries, in order to prevent diseases associated with brain-vasculature remodeling in response to aging and associated comorbidities.
This special issue of Neural Plasticity will provide up-to-date information on molecular, cellular, and behavioral events associated with neurodegenerative diseases and new therapeutic options.
1) Aging, comorbidities, and risk of neurodegenerative diseases and stroke
2) Vascular risk factors for neurodegenerative diseases
3) Aging and vascular risk factors for cognitive decline and dementia
4) Aging and metabolic risk factors for hemorrhagic stroke
5) Brain plasticity and aging
6) Brain plasticity and epilepsy
7) Brain plasticity and neurobehavioral recuperation after cerebral ischemia
Aurel Popa-Wagner and Bogdan Catalin
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