Abstract
The aging process, comorbidities, and age-associated diseases are closely dependent on each other. Cerebral ischemia impacts a wide range of systems in an age-dependent manner. However, the aging process has many facets which are influenced by the genetic background and epigenetic or environmental factors, which can explain why some people age differently than others. Therefore, there is an urgent need to identify age-related changes in body functions or structures that increase the risk for stroke and which are associated with a poor outcome. Multimodal imaging, electrophysiology, cell biology, proteomics, and transcriptomics, offer a useful approach to link structural and functional changes in the aging brain, with or without comorbidities, to post-stroke rehabilitation. This can help us to improve our knowledge about senescence firstly, and in this context, aids in elucidating the pathophysiology of age-related diseases that allows us to develop therapeutic strategies or prevent diseases. These processes, including potential therapeutical interventions, need to be studied first in relevant preclinical models using aged animals, with and without comorbidities. Therefore, preclinical research on ischemic stroke should consider age as the most important risk factor for cerebral ischemia. Furthermore, the identification of effective therapeutic strategies, corroborated with successful translational studies, will have a dramatic impact on the lives of millions of people with cerebrovascular diseases.
Highlights
Studies using electrophysiological techniques, and in particular, electroencephalography (EEG), in ischemic aged animals are quite a few
The models in aged animals have to be designed to (i) create a reproducible lesion which mimics the human pathophysiological changes; (ii) be minimally invasive, and (iii) allow objective measurement and analysis of tissue damage after cerebral ischemia. In agreement with this concept, previous studies have shown that mortality in post-stroke aged rats is higher compared with young animals, most likely because the lesion appears on a background already altered by senescence itself
It was found that there was an inverse neurovascular coupling with SD in the old, but not in the young animals, suggesting thatadaptation of cerebrovascular function with aging impairs the SD-related cerebral blood flow (CBF) response [34]
Summary
Age is the most important risk factor for cerebral ischemia and recovery after cerebral ischemia. The models in aged animals have to be designed to (i) create a reproducible lesion which mimics the human pathophysiological changes; (ii) be minimally invasive, and (iii) allow objective measurement and analysis of tissue damage after cerebral ischemia In agreement with this concept, previous studies have shown that mortality in post-stroke aged rats is higher compared with young animals, most likely because the lesion appears on a background already altered by senescence itself. Experimental evidence suggests that the severity of injury during cerebral ischemia is significantly influenced by age, at structural and functional levels, and at transcriptional levels These age-related changes in the transcriptional activity of brain are associated with an increased vulnerability and reduced functional recovery after focal cerebral ischemia [47]. Middle aged and older mice showed an upregulation of neurogenesis in the contralateral uninjured hemisphere, as opposed to young mice [79]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
