Retraction Note: Chronic neuroinflammation and cognitive impairment following transient global cerebral ischemia: role of fractalkine/CX3CR1 signaling.

This article [1] has been retracted by the Editors-in-Chief. Based on the report of an inquiry conducted by Wayne State University and additional analysis conducted by the Office of Research Integrity (ORI) [2], the ORI informed the journal that the first author Dr Teresita L. Briones engaged in research misconduct by falsifying and/or fabricating data by falsely reporting the results of Western blot experiments, and that data reported in Figures 2A and 2C in [1] were duplicated, reused and falsely relabelled, and claimed to represent different experiments.

Chapter 3 animal models of traumatic brain injury: is there an optimal model that parallels human brain injury?

Traumatic brain injury (TBI) is the leading cause of mortality and morbidity in the younger population worldwide. Survivors of TBI often experience long-term disability in the form of cognitive, sensorimotor, and affective impairments. Despite the high prevalence in, and cost of TBI to, both individuals and society, some of its underlying pathophysiology is not completely understood.

Neuroprotective effects of enriched environment housing after transient global cerebral ischaemia are associated with the upregulation of insulin-like growth factor-1 signalling.

Aims: Use of enriched environment (EE) housing has been shown to promote recovery from cerebral ischaemic injury but the underlying mechanisms of their beneficial effects remains unclear. Here we examined whether the beneficial effects of EE housing on ischaemia-induced neurodegeneration and cognitive impairment are associated with increased insulin-like growth factor-1 (IGF-1) signalling in the hippocampus.

Methods: Forty-two adult male Wistar rats were included in the study and received either ischaemia or sham surgery.

Retracted: Involvement of insulin-like growth factor-1 in chemotherapy-related cognitive impairment.

Here we examined the involvement of insulin-like growth factor 1 (IGF-1) on chemotherapy-induced cognitive impairment. Sixty-four ovariectomized female Sprague-Dawley rats were included in the study and given cyclophosphamide, methothrexate, and 5-fluorouracil (CMF) drug combination or saline (control). CMF was given once a week for 4 weeks.

Chronic neuroinflammation and cognitive impairment following transient global cerebral ischemia: role of fractalkine/CX3CR1 signaling.

Although neuroinflammation has been studied extensively in animal models of cerebral ischemia, their contrasting functions are still not completely understood. A major participant in neuroinflammation is microglia and microglial activation usually regulated by the chemokine CX3CL1 (fractalkine) and its receptor, CX3CR1. Here, we examined the involvement of CX3CR1 on ischemia-induced chronic neuroinflammation and cognitive function using small interfering RNA (siRNA).

Decreased neuroinflammation and increased brain energy homeostasis following environmental enrichment after mild traumatic brain injury is associated with improvement in cognitive function.

Background: Persistent neuroinflammation and disruptions in brain energy metabolism is commonly seen in traumatic brain injury (TBI). Because of the lack of success of most TBI interventions and the documented benefits of environmental enrichment (EE) in enhancing brain plasticity, here we focused our study on use of EE in regulating injury-induced neuroinflammation and disruptions in energy metabolism in the prefrontal cortex and hippocampus. Adult male Wistar rats were used in the study and randomly assigned to receive either: mild TBI (mTBI) using the controlled cortical injury model or sham surgery.

Dysregulation in myelination mediated by persistent neuroinflammation: possible mechanisms in chemotherapy-related cognitive impairment.

Cognitive impairment is commonly reported as a consequence of chemotherapy and can have considerable impact on everyday life on cancer patients. Thus, it is imperative to have a clear understanding of this phenomenon and the underlying mechanism involved. In the present study we examined the role of neuroinflammation and myelination in chemotherapy-related cognitive impairment.

Vitamin D mitigates age-related cognitive decline through the modulation of pro-inflammatory state and decrease in amyloid burden.

Background: Increasing evidence shows an association between the use of vitamin D and improvement in age-related cognitive decline. In this study, we investigated the possible mechanisms involved in the neuroprotective effects of vitamin D on age-related brain changes and cognitive function.

Methods: Male F344 rats aged 20 months (old) and 6 months (young) were used and randomly assigned to either vitamin D supplementation or no supplementation (control).

Chemotherapy-induced cognitive impairment is associated with decreases in cell proliferation and histone modifications.

Background: In this study, we examined the effects of cyclophosphamide, methothrexate, and 5-Fluorouracil (CMF) drug combination on various aspects of learning and memory. We also examined the effects of CMF on cell proliferation and chromatin remodeling as possible underlying mechanisms to explain chemotherapy-associated cognitive dysfunction. Twenty-four adult female Wistar rats were included in the study and had minimitter implantation for continuous activity monitoring two weeks before the chemotherapy regimen was started.

Modulation of ischemia-induced NMDAR1 activation by environmental enrichment decreases oxidative damage.

In this study, we examined whether enriched environment (EE) housing has direct neuroprotective effects on oxidative damage following transient global cerebral ischemia. Fifty-two adult male Wistar rats were included in the study and received either ischemia or sham surgery. Once fully awake, rats in each group were randomly assigned to either: EE housing or socially paired housing (CON).

Environmental experience modulates ischemia-induced amyloidogenesis and enhances functional recovery.

In this study, we examined whether ischemia-induced amyloidogenesis could be modulated by environmental "experience," and whether this modulation is associated with improved cognitive functioning. Rats were subjected to either global ischemia or sham surgery and then were randomly assigned to either enriched environment housing (EE) or socially paired housing (controls). After 14 days of differential environmental housing, the rats were tested in the water maze.

Psychoneuroimmunology and related mechanisms in understanding health disparities in vulnerable populations.

The nervous system as well as the endocrine system maintain extensive communication with the immune system through the influence of hormones and neurotransmitters and also by way of the hardwiring of sympathetic and parasympathetic nerves to the lymphoid organs. There is now convincing evidence that the communication between these three body systems is bidirectional. This chapter will provide a succinct review of how neuroendocrine and immune functions are affected in factors that impact vulnerability, such as aging, acute infection, and central nervous system injury.

Astrocytic changes in the hippocampus and functional recovery after cerebral ischemia are facilitated by rehabilitation training.

In this study we examined whether astrocytic and basic fibroblast growth factor changes after cerebral ischemia can be influenced by rehabilitation training and if these changes are associated with functional improvement. After receiving either ischemia or sham surgery, male adult Wistar rats were assigned to one of two rehabilitation training group: complex environment housing (EC) or paired housing as controls (CON). Rats were tested in the water maze after 14 days of rehabilitation training.

Behaviorally induced synaptogenesis and dendritic growth in the hippocampal region following transient global cerebral ischemia are accompanied by improvement in spatial learning.

Reports have shown that damage to the adult brain can result in adaptive changes in regions adjacent or surrounding the site of the principal injury and that these changes may be modulated by rehabilitation training. In this study, we examined the influence of complex environment housing as a rehabilitation strategy on ischemia-induced synaptic and dendritic changes in the hippocampus. Thirty-six adult male Wistar rats were included in the study and assigned to either transient global cerebral ischemia or sham group.

Environment, physical activity, and neurogenesis: implications for prevention and treatment of Alzhemier's disease.

Age is the biggest risk factor for the development of neurodegenerative diseases. Consequently, as the population ages it becomes more critical to find ways to avoid the debilitating cost of neurodegenerative diseases such as Alzheimer's. Some of the non-invasive strategies that can potentially slow down the mental decline associated with aging are exercise and use of multi-sensory environmental stimulation.

Amelioration of cognitive impairment and changes in microtubule-associated protein 2 after transient global cerebral ischemia are influenced by complex environment experience.

In this study we examined whether expression of microtubule-associated protein 2 (MAP2) after transient global cerebral ischemia can be influenced by behavioral experience and if the changes are associated with functional improvement. Rats received either ischemia or sham surgery then assigned to: complex environment housing (EC) or social housing (SC) as controls for 14 days followed by water maze testing. Upregulation of MAP2 was seen in all ischemic animals with a significant overall increase evident in the EC housed rats.

Changes in number of synapses and mitochondria in presynaptic terminals in the dentate gyrus following cerebral ischemia and rehabilitation training.

Damage to the adult brain can result in adaptive plasticity in regions adjacent to the site of the principal insult and that the plastic changes may be modulated by post-injury rehabilitation training. In this study, we examined the effects of rehabilitation training on synaptic morphology in the dentate gyrus following transient global cerebral ischemia and the metabolic correlates of the ultrastructural changes. Forty adult male Wistar rats were included in the study and assigned to either ischemia or sham group.

Dentate gyrus neurogenesis after cerebral ischemia and behavioral training.

Neurogenesis in the mammalian brain continues throughout adulthood. Several factors have been shown to influence neurogenesis, including experience in a complex environment (EC), exercise (EX), and ischemic insult. The authors investigated the effects of behavioral rehabilitation training following transient global cerebral ischemia on the number of new cells in the dentate gyrus that incorporated bromodeoxyuridine (BrdU), a thymidine analog that labels cells undergoing DNA replication.

Stability of synaptic plasticity in the adult rat visual cortex induced by complex environment exposure.

Studies have demonstrated the effects of complex environment (EC) housing on brain plasticity both during postnatal development and in adulthood, but it is not clear how long these plastic changes persist nor what happens when environmental exposure is discontinued. Here we examined layer IV in the visual cortex of adult male rats for the: (1) effects of EC housing on synaptic plasticity, and (2) persistence of the synaptic changes after withdrawal from the complex environment. Fifty-eight adult male Long Evans rats were assigned to either: EC, socially paired housing (SC), or individual housing (IC).

Behaviorally-induced ultrastructural plasticity in the hippocampal region after cerebral ischemia.

Behavioral training has been shown to induce synaptic plasticity in both intact and injured animals. Because of the possibility that the adaptive changes after ischemic damage may make the brain more malleable to behavioral training, we examined the effects of complex environment (EC) housing and exercise (EX) after global cerebral ischemia on synaptic structural alterations. Forty-two adult male Wistar rats were included in the study and assigned to either ischemia or sham group.