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 panelGuangchiSuna1PengzhanZhaoa1LiangFanbZhongyuanBaoaYimingTuaChongLiaHongluChaoaXiupengXuaJingJia
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.
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