Deferoxamine pre-treatment protects against postoperative cognitive dysfunction of aged rats by depressing microglial activation via ameliorating iron accumulation in hippocampus

Pan, Ke; Li, Xiaojun; Chen, Yan; Zhu, Dan; Li, Yuping; Tao, Guocai; Zuo, Zhiyi

doi:10.1016/j.neuropharm.2016.09.004

Cited by 36 publications

(20 citation statements)

References 64 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Local hepcidin expression in the brain has been an object of investigation of different studies. In physiological conditions hepcidin expression in brain structures and cells (neurons, glial cells, endothelial cells, epithelial cells of choroid plexus) has been consistently observed by in vivo studies in humans and rodents, albeit in low levels ( Krause et al, 2000 ; Pigeon et al, 2001 ; Zechel et al, 2006 ; Wang et al, 2008 , 2010 ; Hänninen et al, 2009 ; Raha et al, 2013 ; Wei et al, 2014 ; Farajdokht et al, 2015 ; Raha-Chowdhury et al, 2015 ; Graf et al, 2016 ; Li Y. et al, 2016 ; Pan et al, 2016 ; Tan et al, 2016 ; Lu et al, 2017 ; You et al, 2017 ; Zhang et al, 2017 ). Data from human and animal studies suggest that local hepcidin is more robustly expressed in pathophysiological states ( Sun et al, 2012 ; Urrutia et al, 2013 ; Tan et al, 2016 ; Xiong et al, 2016 ; You et al, 2017 ; Zhang et al, 2017 ).…”

Section: Brain Hepcidin Expression and Mechanisms Of Regulationmentioning

confidence: 83%

“…It is evident that local and/or systemic hepcidin is induced during brain inflammation and iron load ( Urrutia et al, 2013 ; Xiong et al, 2016 ). In vivo experiments during brain inflammation show that the use of iron chelation protects from brain iron overload, reduces microglial activation and improves cognitive functions in rodents by reducing levels of hepcidin and increasing levels of FPN in hippocampus ( Li Y. et al, 2016 ; Pan et al, 2016 ). In addition, maternal diet and calorie restriction have been proposed as factors that offer neuroprotection by reducing brain iron load through suppression of brain hepcidin ( Wei et al, 2014 ; Graf et al, 2016 ).…”

Section: Dual Role Of Hepcidin In Brain Pathologies; Implications Formentioning

confidence: 99%

“…In animal models with brain inflammation and increased oxidative stress, direct and indirect suppression of local and systemic hepcidin offers neuroprotection ( Chen et al, 2015 ; Li W.-Y. et al, 2016 ; Pan et al, 2016 ; Xiong et al, 2016 ). But, in conditions with lack of inflammation, the use of ad-hepcidin has also beneficial effects in neuronal function, probably due to hepcidin ability to protect neurons during iron overload via suppression of cellular iron import proteins.…”

Section: The Rationale For Using Hepcidin Therapeutics In Neurodegenementioning

confidence: 99%

See 2 more Smart Citations

The Dual Role of Hepcidin in Brain Iron Load and Inflammation

Vela

2018

Front. Neurosci.

View full text Add to dashboard Cite

Hepcidin is the major regulator of systemic iron metabolism, while the role of this peptide in the brain has just recently been elucidated. Studies suggest a dual role of hepcidin in neuronal iron load and inflammation. This is important since neuronal iron load and inflammation are pathophysiological processes frequently associated with neurodegeneration. Furthermore, manipulation of hepcidin activity has recently been used to recover neuronal damage due to brain inflammation in animal models and cultured cells. Therefore, understanding the mechanistic insights of hepcidin action in the brain is important to uncover its role in treating neuronal damage in neurodegenerative diseases.

show abstract

Section: Brain Hepcidin Expression and Mechanisms Of Regulationmentioning

confidence: 83%

Section: Dual Role Of Hepcidin In Brain Pathologies; Implications Formentioning

confidence: 99%

Section: The Rationale For Using Hepcidin Therapeutics In Neurodegenementioning

confidence: 99%

See 1 more Smart Citation

The Dual Role of Hepcidin in Brain Iron Load and Inflammation

Vela

2018

Front. Neurosci.

View full text Add to dashboard Cite

show abstract

“…In preclinical studies, it has been suggested that neuroinflammation drives early POCD, whereas resolution of neuroinflammation could allow reversal of POCD (20). In a separate study, it has been shown that oxidative stress induced by hippocampal iron accumulation might induce cognitive impairment in a rat model of POCD (21). A more recent study suggested that surgery-induced Ang II release impairs blood-brain barrier integrity by activating NF-κB signaling pathway, which might contribute to the development of POCD (22).…”

Section: Mechanisms Underlying Pocdmentioning

confidence: 99%

Postoperative Cognitive Dysfunction: Knowns and Unknowns

Ji¹,

Su²,

Yang³

2017

J Anesth Perioper Med

View full text Add to dashboard Cite

Aim of review: The aim of this review was to summarize and discuss current status and challenges in our understanding of the diagnosis, risk factors, pathophysiologic mechanisms, and preventions for postoperative cognitive dysfunction (POCD). Method: We searched and reviewed the articles about POCD published in the past 2 decades using PubMed and Google Scholar. Recent findings: POCD affects a wide variety of cognitive domains, including attention, memory, executive function and speed of information processing, with the deficits in memory and a reduced ability to handle intellectual challenges being most obvious. The causes of POCD are thought to be multifactorial and may include the preoperative health status of the patient, the patients' preoperative level of cognition, perioperative events related to the surgery itself, and possible neurotoxic effects of anesthetic agents. There are many controversies about POCD, from how it is measured to how long it lasts, to its precise implications for patients, and whether POCD is linked to a long-term risk of developing dementia. Summary: POCD is a topic of special importance in the geriatric surgical population. Unfortunately, no therapeutic interventions are available to prevent the onset of POCD, strategies for management of these patients should be a multimodal approach involving close cooperation between the anesthesiologist, surgeon, geriatricians, and family members to promote early rehabilitation and avoid loss of independence in these patients. Future researches focusing on the mechanisms involved in POCD are critical for better understanding and management of this cognitive dysfunction after surgery.

show abstract

“…The required for full microglial activation [44]. They found that they were able to stave off microglia activation by oxidative stress mechanisms, using deferoxamine, and were also able to prevent the associated neurotoxicity and cognitive defi cits.…”

Section: How Volatile General Anesthetics (Vga) Can Induce Ad Pathologymentioning

confidence: 99%

Can Exposure to Volatile Anesthetics Be a Tipping Point for AD Susceptible Populations?

Niesman¹

2017

Ann Alzheimers Dement Care

View full text Add to dashboard Cite

The relationship between surgery induced Postoperative Cognitive Dysfunction (POCD) and the development of Alzheimer's disease (AD) later has been a debatable question. Volatile anesthetics represent a potential environmental factor that can change the CNS both acutely and long-term. By interacting with membrane cholesterol to alter signaling in neurons or alter the normally quiescent microglial phenotype, volatile anesthetics are implicated in the development of POCD. The tipping point for triggering AD cyclic pathology may rest with individual AD genetic risk factors combined with the known molecular consequences of anesthetic exposure. This review covers genome wide association studies (GWAS) identifi ed AD risk factors, actions of volatile anesthetics in the development of AD phenotypes and presents some newly discovered pre or post-anesthetic POCD attenuating therapies.

show abstract

Deferoxamine pre-treatment protects against postoperative cognitive dysfunction of aged rats by depressing microglial activation via ameliorating iron accumulation in hippocampus

Cited by 36 publications

References 64 publications

The Dual Role of Hepcidin in Brain Iron Load and Inflammation

The Dual Role of Hepcidin in Brain Iron Load and Inflammation

Postoperative Cognitive Dysfunction: Knowns and Unknowns

Can Exposure to Volatile Anesthetics Be a Tipping Point for AD Susceptible Populations?

Contact Info

Product

Resources

About