Tuesday, October 18, 2016

What Do We Remember ?

https://www.scientificamerican.com/article/trying-to-forget-may-impair-memory/
              Go ahead. Try it. What did you have for breakfast last Tuesday? Oatmeal, eggs, waffles? Did you, perhaps, skip breakfast because you didn’t hear your alarm go off or you took a little too long in the shower? If you are like me, and most other humans for that matter, you may draw a complete blank when asked these seemingly simple questions. If you are like me, you may even be totally and utterly convinced of a particular aspect of a situation that your memory tells you is true, but ends up being dead wrong. If you are like me, you may wonder just how specific details become lost in the routines of daily life. If you are like me, you may wonder why exactly some particulars are salient and others become muddled in the sea of memories that our brain is forced to process. If you are like me, you will be intrigued to find out why we can or cannot remember whether or not we had pancakes, a side of orange juice, and an apple for breakfast last Tuesday morning.
 In the article “Neural Correlates of Reactivation and Retrieval-Induced Learning,” Bridge and Paller of Northwestern University discuss how recall of recently learned information can be improved via reactivation of this information, just like what you had for breakfast this morning. They supported this theory with an experiment which involved three trials that tested participants’ memory of 180 object-location associations over 72 hours (in 24 hour increments). Participants were provided with a grid in which an object would appear in the middle, and then be placed in a certain location on the grid (see figure). They learned these associations until they could correctly place all the objects twice. This simulates newly learned facts in our everyday lives, such as how many pounds are in a kilogram, or how many plays Shakespeare wrote. In trials 1 and 3, participants were asked to recall spatial associations for all 180 items. However, in trial 2, participants were only asked to place a subset of the items in their correct locations, while the others merely flashed in the middle of the screen. The researchers hypothesized that, because participants were being asked to recall the location of the items in trial 2 with a greater frequency than the items not included in trial 2, participants would demonstrate a greater accuracy of recall for those items in trial 3. This means that the subjects’ memory was better for objects that they had reactivated in their memories. As they had predicted, retrieval of the items in session 2 led to significantly greater recall accuracy in trial 3 when compared with the items that the participants had not been asked to recall in trial 2. For those of us who remember studying history in grade school, this makes sense. The more we recall new facts, such as the day the Constitution was signed or the name of the Union general at the beginning of the Civil War, the more readily we are able to recall them at a later time. Finally, we are validated for those countless hours sitting at the kitchen table with our noses buried in a history book!
Furthermore, Bridge and Pallor also explored what happens if we retrieve information but that information is actually inaccurate with respect to the information we had actually learned in the first place. Imagine this, you are sitting at your kitchen table studying history. You read in your book that the Constitution was signed in1787, but your mom walks in and mistakenly declares that it was actually signed in1776. You write this down on a notecard for further studying and you ultimately get this question wrong on the test because you retrieved inaccurate information.  Bridge and Pallor found similar results to this scenario. If participants incorrectly recalled a location in trial 2, they were significantly more likely to place the item in trial 3 near the incorrect trial 2 location than in the correct trial 1 location. Therefore, to this reader, it seems logical that inaccuracies in memory may accumulate over subsequent recalls, potentially leading to a false memory. It truly forces one to wonder how well the most vivid memories compare to what had occurred in reality. Is our view of the past actually just a product of numerous distortions?
However, what happens when we deliberately try to suppress information? Is it actually possible to forcibly forget? A recent study by Jesse Rissman addressed this exact question. Participants were asked to memorize sets of word pairs, with one word being linked to a set of retrieval tasks and the other being linked to a set of suppression tasks. Participants were also shown a picture of an object in a specific background (a teddy bear in a kitchen, for example) in between these retrieval and suppression tasks and asked to relate the picture to the word pair. Interestingly, when later asked to recall the object when given the location without the object in it (i.e. just the kitchen), participants were significantly more likely to correctly identify the object (i.e. teddy bear) when the object/background pair was given between retrieval tasks than between suppression tasks. Clearly, it is possible that forcible memory suppression hinders future recall. This fact could possibly explain why people suffering from PTSD oftentimes have issues with short-term memory, as they oftentimes repress their traumas. 

Clearly, there is no need to tie a ribbon around your finger the next time you have to remember to send a birthday card to your grandmother or pick up some milk from the grocery store. Just remember, constant and consistent retrieval is key! Maybe you will even start to remember what you had to breakfast last Tuesday.

Works Cited
Bridge, Donna A. and Ken A. Paller. "Neural Correlates of Reactivation and Retrieval-Induced Distortion." Journal of Neuroscience 32.35 (2012): 12144-12155.
Sachan, Disna. "Trying to Forget May Impair Memory." Scientific American. N.p., 02 Aug. 2016. Web. 17 Oct. 2016


B


Oxidative Stress in Neurodegenerative Diseases:


Parkinson's disease and Alzheimer's disease

http://popwrapped.com/wp-content/uploads/2016/07/alzehimer.jpg
Parkinson’s disease is the most common neurodegenerative movement disorder and the second most common neurodegenerative disease in developed countries. This disease is characterized by a loss of dopamine neurons in the Substantia nigra that are needed for proper motor function. As a result, those who suffer from this disorder develop tremors and muscle rigidity.
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In “Calcium, Cellular Aging, and Selective Neuronal Vulnerability inParkinson’s Disease,” D. James Surmeier and his colleagues focused on the dopamine neurons of the Substantia nigra (SNc DA Neurons) and why they die. It is hypothesized that the primary factor for their deaths is stress created by sustained Calcium entry which leads to compromised oxidative defenses, amongst other injuries. Also, reactive oxygen species (ROS) are easily converted into free radicals which are chemical species that have unpaired electrons in their outer orbit. They can be harmful by causing mutations in SNc DA neurons which can trigger neuron degeneration and apoptosis. Parkinson’s disease is thought to be a result of this accelerated aging and oxidative stress in selective neural systems.

Oxidative Stress:
     A similar hypothesis concerning oxidative stress was made by Manuela Padurariu and her colleagues with regards to Alzheimer’s disease. In general, oxidative-stress-related injuries are caused by an imbalance between pro-oxidants and anti-oxidants. Specifically, an excess of pro-oxidant compounds triggers antioxidant defenses that deplete the body’s antioxidant reserves through reduction of the antioxidants to harmful free radicals. These free radicals can attack cellular structures such as DNA, RNA, proteins, and lipids in the cellular membrane. Less aggressive free radicals cause easily repairable lesions, but more aggressive types can be mutagenic and highly cytotoxic. In turn, oxygen radicals can cause cancer and neurological diseases such as Parkinson’s disease, Huntington’s disease, and Alzheimer’s disease.

https://authoritynutrition.com/wp-content/uploads/2014/10/antioxidants-vs-free-radicals.jpg
     The brain is especially vulnerable to oxidative stress because of its low levels of antioxidants, high concentration of the lipids free radicals attack via lipidic peroxidation, and its high biochemical oxygen demand. The most vulnerable areas in the brain are in the hippocampus, a highly active part of the brain. This is because the most active neurons already have intrinsic oxidative stress due to their high bioenergetics needs and, therefore, they have a greater number of mitochondria that are vulnerable to additional oxidative stress. An accumulation of ROS in Alzheimer’s disease may be the earliest sign of risk of developing the disease. Theories about the accumulation of ROS in Alzheimer’s disease relate to dysfunctions in the mitochondria that lead to the production of more ROS and amyloid beta plaques – a characteristic of Alzheimer’s disease – which activates microglia and leads to more ROS. Also, an overconsumption of antioxidants is thought to lead to the reduction of these antioxidants to free radicals, resulting in a positive feedback loop. Although the mitochondria’s role in Alzheimer’s disease is not fully understood yet, it is thought to be the central cause.

Antioxidant Therapy:
http://www.foodinsight.org/sites/default/files/field/image/antiox.jpg

     Antioxidant compounds may help reduce amyloid beta toxicity. Blueberries, melatonin, Gingko biloba extracts and other supplements contain these antioxidant compounds. The most important soluble antioxidant is Vitamin C because it neutralizes ROS before lipidic peroxidation can occur. Vitamin E also protects membrane lipids from lipidic peroxidation. While these antioxidants may assist in treatment and prevention of Alzheimer’s disease, further research regarding this type of therapy is needed (especially in early stages of Alzheimer’s type dementia) to prove that there is a clear benefit. With the help of biomarkers and more research on the effects of oxidative stress in age-related neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease, more treatment options and prevention techniques may become available.

Sources:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3235732/pdf/nihms168524.pdf

http://www.hdbp.org/psychiatria_danubina/pdf/dnb_vol25_no4/dnb_vol25_no4_401.pdf

http://ac.els-cdn.com/S0925443913003232/1-s2.0-S0925443913003232-main.pdf?_tid=783a2380-9338-11e6-b117-00000aab0f01&acdnat=1476578322_daef3fafa75f824388ea849804c416c5