Blueberry Supplementation Mitigates Altered Brain Plasticity and Behavior after Traumatic Brain Injury in Rats

Abstract

Scope Traumatic brain injury (TBI) compromises neuronal function required for hippocampal synaptic plasticity and cognitive function. Despite the high consumption of blueberries, information about its effects on brain plasticity and function under conditions of brain trauma is limited. The efficacy of dietary blueberry (BB) supplementation to mitigate the effects of TBI on plasticity markers and associated behavioral function in a rodent model of concussive injury are assessed. Methods and results Rats were maintained on a diet supplemented with blueberry (BB, 5% w/w) for 2 weeks after TBI. It is found that BB supplementation mitigated a loss of spatial learning and memory performance after TBI, and reduced the effects of TBI on anxiety‐like behavior. BB supplementation prevents a reduction of molecules associated with the brain‐derived neurotrophic factor (BDNF) system action on learning and memory such as cyclic‐AMP response element binding factor (CREB), calcium/calmodulin‐dependent protein kinase II (CaMKII). In addition, BB supplementation reverses an increase of the lipid peroxidation byproduct 4‐hydroxy‐nonenal (4‐HNE) after TBI. Importantly, synaptic and neuronal signaling regulators change in proportion with the memory performance, suggesting an association between plasticity markers and behavior. Conclusion Data herein indicate that BB supplementation has a beneficial effect in mitigating the acute aspects of the TBI pathology.

Nrf2/HO-1 mediates neuroprotective effects of pramipexole by attenuating oxidative damage and mitochondrial perturbation after traumatic brain injury

“…4-HNE is a toxic aldehydic by-product of LPO and a biomarker of oxidative stress. Increased levels of 4-HNE indicate more serious oxidative damage in TBI pathogenesis as reported by Krishna et al (2019) .…”

Approaches to Monitor Circuit Disruption after Traumatic Brain Injury: Frontiers in Preclinical Research

“…Animal models have extended clinical findings to show impaired neuroplasticity after diffuse TBI [45]. Neural plasticity is highly adaptive and works to maintain the homeostatic processes by recruiting neurotrophic factors which compensate for the injury-induced adaptations [46,47].…”

Nutritional interventions to improve neurophysiological impairments following traumatic brain injury: A systematic review

“…Anti‐oxidant compounds α‐lipoic acid (ALA) (Ozbal et al., 2015; Toklu et al., 2009; Wei et al., 2015), catechin (Jiang et al., 2017), (‐)‐epicatechin(Cheng et al., 2016), and astaxanthin (Ji et al., 2017) were delivered via oral gavage. In the remaining studies, animals received (–)‐epigallocatechin gallate (EGCG) dissolved in drinking water (Itoh et al., 2013), and a diet enriched with blueberries (Krishna et al., 2019). In each study the intervention was initiated within 3 hr of TBI.…”