Influence of age on stroke outcome following transient focal ischemia

Rosen, Charles L.; DiNapoli, Vincent; Nagamine, Tomoaki; Crocco, Todd J.

doi:10.3171/jns.2005.103.4.0687

Cited by 73 publications

(74 citation statements)

References 35 publications

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“…The behavioral outcome in aged animals has been reported to be impaired compared with young animals (Zhang et al, 2005;Popa-Wagner et al, 2007;Petcu et al, 2008). The effect of age on the infarct size in preclinical studies has resulted in somewhat contradictory findings depending on the ischemia model used (Davis et al, 1995;Kharlamov et al, 2000;Shapira et al, 2002;Rosen et al, 2005). In this current study, the infarct size in aged mice was similar compared with young mice, a finding that is in agreement with a previously published study using a photothrombotic model of brain ischemia (Zhao et al, 2005).…”

Section: Discussionsupporting

confidence: 90%

Aging aggravates ischemic stroke-induced brain damage in mice with chronic peripheral infection

et al. 2013

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SummaryIschemic stroke is confounded by conditions such as atherosclerosis, diabetes, and infection, all of which alter peripheral inflammatory processes with concomitant impact on stroke outcome. The majority of the stroke patients are elderly, but the impact of interactions between aging and inflammation on stroke remains unknown. We thus investigated the influence of age on the outcome of stroke in animals predisposed to systemic chronic infection. Th1-polarized chronic systemic infection was induced in 18-22 month and 4-month-old C57BL/6j mice by administration of Trichuris muris (gut parasite). One month after infection, mice underwent permanent middle cerebral artery occlusion and infarct size, brain gliosis, and brain and plasma cytokine profiles were analyzed. Chronic infection increased the infarct size in aged but not in young mice at 24 h. Aged, ischemic mice showed altered plasma and brain cytokine responses, while the lesion size correlated with plasma prestroke levels of RANTES. Moreover, the old, infected mice exhibited significantly increased neutrophil recruitment and upregulation of both plasma interleukin-17a and tumor necrosis factor-a levels. Neither age nor infection status alone or in combination altered the ischemia-induced brain microgliosis. Our results show that chronic peripheral infection in aged animals renders the brain more vulnerable to ischemic insults, possibly by increasing the invasion of neutrophils and altering the inflammation status in the blood and brain. Understanding the interactions between age and infections is crucial for developing a better therapeutic regimen for ischemic stroke and when modeling it as a disease of the elderly.

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Section: Discussionsupporting

confidence: 90%

Aging aggravates ischemic stroke-induced brain damage in mice with chronic peripheral infection

et al. 2013

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“…In fact, several studies have revealed an impairment in regeneration after brain injury in the aged brain (Popa-Wagner et al, 2009). Young rats recover more quickly than aged rats and undergo complete functional recovery following ischemic cortical injury, whereas aged animals only recover approximately 70% of their pre-stroke motor function (Rosen et al, 2005;Buga et al, 2008). Further highlighting the need to perform studies in appropriate age cohorts is the recent finding that apocynin (a NOX2 inhibitor) administration, a therapy that promotes recovery by reducing oxidative stress following stroke injury in young rats, leads to reduced functional recovery in aged rats (Kelly et al, 2009).…”

Section: Disease Models and Mechanisms 423mentioning

confidence: 99%

Potential and pitfalls of stem cell therapy in old age

Piccin

Morshead

2010

Disease Models &Amp; Mechanisms

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Our increasing understanding of resident stem cell populations in various tissues of the adult body provides promise for the development of cell-based therapies to treat trauma and disease. With the sharp rise in the aging population, the need for effective regenerative medicine strategies for the aged is more important then ever. Yet, the vast majority of research fuelling our understanding of the mechanisms that control stem cell behaviour, and their role in tissue regeneration, is conducted in young animals. Evidence collected in the last several years indicates that, although stem cells remain active into old age, changes in the stem cells and their microenvironments inhibit their regenerative potential. An understanding of both the cell-intrinsic stem cell changes, as well as concomitant changes to the stem cell niche and the systemic environment, are crucial for the development of regenerative medicine strategies that might be successful in aged patients.

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“…While some studies show that the immature brain is more vulnerable to brain damage resulting from stroke [73], others have suggested that increasing age has no effect on stroke volume [74], or may worsen infarct size [75]. Nevertheless, age affects many of the molecular processes commonly associated with neuroplasticity and stroke recovery.…”

Section: Therapeutic Interventions Across the Lifespanmentioning

confidence: 99%

Exercise and Environmental Enrichment as Enablers of Task-Specific Neuroplasticity and Stroke Recovery

et al. 2016

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Improved stroke care has resulted in greater survival, but >50 % of patients have chronic disabilities and 33 % are institutionalized. While stroke rehabilitation is helpful, recovery is limited and the most significant gains occur in the first 2-3 months. Stroke triggers an early wave of gene and protein changes, many of which are potentially beneficial for recovery. It is likely that these molecular changes are what subserve spontaneous recovery. Two interventions, aerobic exercise and environmental enrichment, have pleiotropic actions that influence many of the same molecular changes associated with stroke injury and subsequent spontaneous recovery. Enrichment paradigms have been used for decades in adult and neonatal animal models of brain injury and are now being adapted for use in the clinic. Aerobic exercise enhances motor recovery and helps reduce depression after stroke. While exercise attenuates many of the signs associated with normal aging (e.g., hippocampal atrophy), its ability to reverse cognitive impairments subsequent to stroke is less evident. It may be that stroke, like other diseases such as cancer, needs to use multimodal treatments that augment complimentary neurorestorative processes.

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Influence of age on stroke outcome following transient focal ischemia

Cited by 73 publications

References 35 publications

Aging aggravates ischemic stroke-induced brain damage in mice with chronic peripheral infection

Aging aggravates ischemic stroke-induced brain damage in mice with chronic peripheral infection

Potential and pitfalls of stem cell therapy in old age

Exercise and Environmental Enrichment as Enablers of Task-Specific Neuroplasticity and Stroke Recovery

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