MOTW

Summary: The purpose of this study was to evaluate the effect caffeine has on memory. The apparatus used to determine memory and recall was the Auditory Verbal Learning Test (AVLT). Prior to any testing, participants took a personality questionnaire. They were separated into two groups and presented with a list of words (14 words on each list), which they were tasked with memorizing. They were introduced to three lists and asked to recall the items on each. This was done before and after the caffeine was administered. Every time a new list was introduced, they were tasked with memorizing the words in the new list, asked to recall them, and then asked to recall words from the previous list. It was found that as time went on, people who were given caffeine had a harder time recalling words on newly introduced lists (lists 2 and 3), specifically on words 5-14. A correlation was seen between people with anxiety and memory. According to the personality test, people with anxiety tended to have better memory, than those without anxiety. However, people with anxiety, who also were given caffeine, tended to have a worse memory. 

2. 

Jennifer N. Pearson, Shane Rowley, Li-Ping Liang, Andrew M. White, Brian J. Day, Manisha Patel, Reactive oxygen species mediate cognitive deficits in experimental temporal lobe epilepsy, Neurobiology of Disease, Volume 82, 2015, Pages 289-297.

Summary: The purpose of this study was to evaluate if using antioxidants to reduce ROS in rats, with epilepsy, would lessen the severity of the comorbidities caused by seizures. The comorbidity examined in this study is memory, specifically object recognition and spatial memory, which is associated with the hippocampus. Rats were given pilocarpine to induce status epilepticus and then the control group was treated with saline and the experimental group was treated with a synthetic catalytic antioxidant, porphyrin. The rats completed two tasks one being a maze and object recognition. It was found that increases in oxidative stress caused by the pilocarpine were significantly reduced in rats treated with porphyrin. Additionally, rats treated with the antioxidant, had significantly better long-term, short term and spatial memory even after discontinuation of treatment. This suggests that ROS production may be an important driver in deficits associated with epilepsy. 

4. Lesions

Wu, Aiguo, et al. “Vitamin E protects against oxidative damage and learning disability after mild traumatic brain injury in rats.” Neurorehabilitation and Neural Repair, vol. 24, no. 3, 2009, pp. 290–298, https://doi.org/10.1177/1545968309348318.

Summary:  Oxidative Stress is thought to cause cognitive dysfunction and affect neuroplasticity by disrupting the brain-derived neurotrophic factor (BDNF) function. Oxidative Stress can be amplified by traumatic brain injury, but may be rectified by diet, specifically a diet rich in vitamin E. The purpose of this study was to access the ability of vitamin E to protect the BDNF system from oxidative stress. Male were randomly assigned to two groups, one group had the normal chow with 50 IU/kg vitamin E supplement and the other with 500 IU/kg of vitamin E supplement for four weeks Then both groups were given a fluid percussion injury and then their cognitive abilities were assessed by having them complete a water maze. It was found that vitamin E can provide protection from cognitive impairment following a traumatic brain injury (TBI). Vitamin E showed significant improvement in cognition with shorter latency to find the platform compared with untreated TBI animals however, there was no significant difference in swimming speed. It was found that TBI resulted in reduced CaMKII, however rats with the vitamin E diet has elevated levels. Vitamin E supplementation significantly increased levels of CREB in TBI rats as compared with the levels in untreated TBI rats. TBI reduced SOD, whereas vitamin E increased the levels of SOD. TBI resulted in reduced Sir2 in rats fed a RD. Vitamin E elevated the levels of Sir2. 


5. Animal Behavior

Cechetti, Fernanda, et al. “Forced treadmill exercise prevents oxidative stress and memory deficits following chronic cerebral hypoperfusion in the rat.” Neurobiology of Learning and Memory, vol. 97, no. 1, 2012, pp. 90–96, https://doi.org/10.1016/j.nlm.2011.09.008.

Summary: A study was conducted with rats to see if continual exercise impacted both reference and working memory in rats with cerebral hypoperfusion. Both hypoperfusion and oxidative stress have been known to contribute to the development and progression of neurodegenerative diseases such as Alzheimer's Disease and Dementia both of which have an effect on learning and memory. This study was done in rats, in which both carotid arteries were separated from the vagus nerve and occluded with a 5-0 silk suture to induce hypoperfusion. There were three exercise groups (preop, postop and pre+post op) as well as one group that did not exercise (left on a treadmill for 5 mins w/o running stimulus). Rats that exercised, ran for 20 mins, 3 times a week, the speeds progressively each week (for a total of 12 weeks) The exercise intensity was set at 60% of animal’s maximal oxygen uptake, which was determined by having the rats. run on the treadmill at a low initial speed followed by increases of 5 m/min every 3 min until the point of exhaustion; the time to fatigue (in min) and workload (in m/min) were taken as indexes of exercise capacity that were taken as VO2 max. Three months post-op, rats were tested on memory both reference and working. For reference memory, rats were placed in a pool, facing the wall, and had to find the platform. Then the platform was removed and they had to find the spot where the platform should have been. For working memory, the same technique was used, however the platform remained in the pool but moved for each trial. It was found that forced treadmill running protects from spatial learning and memory deficits in 2VO rats when applied to either post- and pre + - post ischemia. Lipid peroxidation was significantly increased after chronic cerebral hypoperfusion Exercise did not alter the levels of basal free radicals in the hippocampus but increased the levels of antioxidants such as thiols and TBARS. On the other hand, there are also studies where swimming and treadmill training did not affect brain antioxidant defenses. It is proposed that exercise, through its continuous free radical generating effect, thus induces the adaptation of the cellular antioxidant system.