Curcumin alleviates neuroinflammation, enhances hippocampal neurogenesis, and improves spatial memory after traumatic brain injury

WHOM THE HELL do we go to to get this tested for stroke and in humans? I want SPECIFIC NAMES that will take responsibility for followthru.

Curcumin alleviates neuroinflammation, enhances hippocampal neurogenesis, and improves spatial memory after traumatic brain injury

Author links open overlay panelGuangchiSun^a1PengzhanZhao^a1LiangFan^bZhongyuanBao^aYimingTu^aChongLi^aHongluChao^aXiupengXu^aJingJi^a

https://doi.org/10.1016/j.brainresbull.2020.05.009Get rights and content

Highlights

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Curcumin rescued spatial memory after TBI in rats.

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Curcumin decreased TBI-induced chronic neuroinflammation.

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Curcumin increased hippocampal neurogenesis after TBI.

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Curcumin may regulate these changes via the BNDF/Trkb/PI3K/AKT pathway.

Abstract

Cognitive decline is one of the most obvious symptoms of traumatic brain injury (TBI). Previous studies have demonstrated that cognitive decline is related to substantially increased neuroinflammation and decreased neurogenesis in the hippocampus in a rat model of TBI. Using this model, we explored the role of curcumin (Cur) in ameliorating TBI-impaired spatial memory because Cur has been shown to exhibit anti-chronic-neuroinflammatory, neurogenesis-promoting, and memory-improving properties.

Animals received daily Cur or vehicle treatment for 28 days after TBI and also received 50-bromodeoxyuridine(BrdU) for the first 7 days of the treatment for assaying neurogenesis. An optimal Cur dose of 30 mg/kg, selected from a range of 10–50 mg/kg, was used for the present study. Neuroinflammation was evaluated by astrocyte hypertrophy, activated microglia, and inflammatory factors in the hippocampus. Behavioral water-maze studies were conducted for 5 days, starting at 35-day post-TBI. The tropomyosin receptor kinase B (Trkb) inhibitor, ANA-12, was used to test the role of the brain-derived neurotrophic factor (BDNF)/ TrkB/Phosphoinositide 3-kinase (PI3K)/Akt signaling pathway in regulating inflammation and neurogenesis in the hippocampus.

Treatment with Cur ameliorated the spatial memory of TBI rats, reduced TBI-induced chronic inflammation, typified by diminished astrocyte hypertrophy, reduction in activated microglia, declined inflammatory factors, and increased neurogenesis in the hippocampus. We also found that BDNF/Trkb/PI3K/Akt signaling was involved in the effects of Cur in TBI rats.

Thus, Cur treatment can ameliorate the spatial memory in a murine model of TBI, which may be attributable to decreased chronic neuroinflammation, increased hippocampal neurogenesis, and/or BDNF/Trkb/PI3K/Akt signaling.

Transcranial Direct Current Stimulation in Stroke Rehabilitation: Present and Future

Don't just lazily write that results have been inconclusive and future studies needed.  Make them conclusive. Isn't that what research is about? And you ARE A RESEARCHER? 

Which tDCS?

• HD-tDCS (3)

• cathodal tDCS (6)   

• anodal tDCS (9)

Transcranial Direct Current Stimulation in Stroke Rehabilitation: Present and Future

• Authors
• Authors and affiliations

• Oluwole O. Awosika
• Leonardo G. Cohen

• Oluwole O. Awosika
  • 1
  • 2
  Email author
• Leonardo G. Cohen
  • 1

1. 1.Human Cortical Physiology and Stroke Neurorehabilitation SectionNational Institutes of HealthBethesdaUSA
2. 2.Department of Neurology and Rehabilitation MedicineUniversity of Cincinnati College of MedicineCincinnatiUSA

Chapter

First Online: 24 January 2019

• 10 Downloads

Abstract

Stroke is the leading cause of severe lasting adult disability around the world. Despite efforts to standardize post-stroke care and rehabilitation a significant percentage of patients remain permanently disabled. Life expectancy after stroke is on the rise in part due to improvements in health care. Hence, it is necessary to develop cost efficient ways to improve the beneficial effects of customary neurorehabilitative interventions (i.e., physical and occupational therapy) on motor and cognitive function after stroke. Over the years, transcranial direct current stimulation has emerged as a possible neuromodulatory tool adjuvant to standard neurorehabilitative therapy. Recent meta-analysis suggested moderate beneficial effects of tDCS on motor function after stroke. However, results from clinical trials have not been conclusive, suggesting the need to understand mechanisms underlying tDCS effects, including optimal stimulation protocols, timing, duration and magnitude of stimulation, and the identification of patient groups more amenable to tDCS effects. Here we discuss study results (organized by functional deficits) to date and discuss critically available evidence. Future studies could benefit from tighter experimental designs, more detailed description of methodologies, preregistration when appropriate and enhanced replication efforts.

Dietary salt promotes ischemic brain injury and is associated with parenchymal migrasome formation

If salt is so bad then write up a diet protocol on it and get it distributed worldwide. Not doing so means you have no followthru and this writeup was worthless. 

Dietary salt promotes ischemic brain injury and is associated with parenchymal migrasome formation

Schmidt-Pogoda A¹, Strecker JK¹, Liebmann M¹, Massoth C², Beuker C¹, Hansen U³, König S⁴, Albrecht S¹, Bock S¹, Breuer J¹, Sommer C⁵, Schwab N¹, Wiendl H¹, Klotz L¹, Minnerup J¹.

Author information

Abstract

Sodium chloride promotes vascular fibrosis, arterial hypertension, pro-inflammatory immune cell polarization and endothelial dysfunction, all of which might influence outcomes following stroke. But despite enormous translational relevance, the functional importance of sodium chloride in the pathophysiology of acute ischemic stroke is still unclear. In the current study, we show that high-salt diet leads to significantly worse functional outcomes, increased infarct volumes, and a loss of astrocytes and cortical neurons in acute ischemic stroke. While analyzing the underlying pathologic processes, we identified the migrasome as a novel, sodium chloride-driven pathomechanism in acute ischemic stroke. The migrasome was previously described in vitro as a migrating organelle, which incorporates and dispatches cytosol of surrounding cells and plays a role in intercellular signaling, whereas a pathophysiological meaning has not been elaborated. We here confirm previously reported characteristics of the migrasome in vivo. Immunohistochemistry, electron microscopy and proteomic analyses further demonstrate that the migrasome incorporates and dispatches cytosol of surrounding neurons following stroke. The clinical relevance of these findings is emphasized by neuropathological examinations, which detected migrasome formation in infarcted brain parenchyma of human stroke patients. In summary, we demonstrate that high-salt diet aggravates stroke outcomes, and we characterize the migrasome as a novel mechanism in acute stroke pathophysiology.

PMID:

30589884

DOI:

10.1371/journal.pone.0209871

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