IMR Press / JIN / Special Issues / 1617167997831

Translational bottleneck for stroke therapy: impact of aging and co-morbidities

Submission deadline: 30 December 2021
Special Issue Editor
  • Aurel Popa-Wagner, MD
    Department of Neurology, Chair of Vascular Neurology, Dementia and Ageing Research, University Hospital Essen, Essen, Germany
    Interests: Aged animals models of cerebral ischemia; Behavioral analysis; Recording of EEG and various physiological parameters by telemetric measurements; MRI for small animals; Immunohistochemical procedures, proteomics, genomics
Special Issue Information

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 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. The main opponent of brain plasticity in the aged brain is neuroinflammation. With increasing age, the brain It is becoming evident that subtle but continuous neuroinflammation can provide the ground for disorders such as cerebral small vessel disease (cSVD) and subsequently 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 ground for further cerebrovascular events; thus, a vicious cycle develops. We also cover brain vasculature recent advances in signaling pathways that can potentially protect cells as well as treatment options for the maintenance of brain capillaries to prevent diseases associated with brain vasculature remodeling in response to aging and associated comorbidities.
This Special Issue will provide an up-to-date information on molecular, cellular, and behavioral events associated with neurodegenerative diseases and new therapeutic options.

Prof. Dr. Aurel Popa-Wagner

Guest Editor

Keywords
Aging
Neurodegenerative diseases
Co-morbidities
Vascular risk Factors
Neuroinflammation
Genomics
Proteomics
Behavioral recovery
Therapies
Manuscript Submission Information

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Published Paper (1 Paper)
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