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- Member of: Theses and Dissertations
The purpose of this study is to know whether the primary motor cortex (M1) plays a role in the sensorimotor memory. It was hypothesized that temporary disruption of the M1 following the learning to minimize a tilt using a ‘L’ shaped object would negatively affect the retention of sensorimotor memory and thus reduce interference between the memory acquired in one context and the visual cues to perform the same task in a different context.
Significant findings were shown in blocks 1, 2, and 4. In block 3, subjects displayed insignificant amount of learning. However, it cannot be concluded that there is full interference in block 3. Therefore, looked into 3 effects in statistical analysis: the main effects of the blocks, the main effects of the trials, and the effects of the blocks and trials combined. From the block effects, there is a p-value of 0.001, and from the trial effects, the p-value is less than 0.001. Both of these effects indicate that there is learning occurring. However, when looking at the blocks * trials effects, we see a p-value of 0.002 < 0.05 indicating significant interaction between sensorimotor memories. Based on the results that were found, there is a presence of interference in all the blocks but not enough to justify the use of TMS in order to reduce interference because there is a partial reduction of interference from the control experiment. It is evident that the time delay might be the issue between context switches. By reducing the time delay between block 2 and 3 from 10 minutes to 5 minutes, I will hope to see significant learning to occur from the first trial to the second trial.
Traumatic brain injury (TBI) is defined as an injury to the head that disrupts normal brain function. TBI has been described as a disease process that can lead to an increased risk for developing chronic neurodegenerative diseases, like frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS). A pathological hallmark of FTLD and a hallmark of ALS is the nuclear mislocalization of TAR DNA Binding Protein 43 (TDP-43). This project aims to explore neurodegenerative effects of TBI on cortical lesion area using immunohistochemical markers of TDP-43 proteinopathies. We analyzed the total percent of NEUN positive cells displaying TDP-43 nuclear mislocalization. We found that the percent of NEUN positive cells displaying TDP-43 nuclear mislocalization was significantly higher in cortical tissue following TBI when compared to the age-matched control brains. The cortical lesion area was analyzed for each injured brain sample, with respect to days post-injury (DPI), and it was found that there were no statistically significant differences between cortical lesion areas across time points. The percent of NEUN positive cells displaying TDP-43 nuclear mislocalization was analyzed for each cortical tissue sample, with respect to cortical lesion area, and it was found that there were no statistically significant differences between the percent of NEUN positive cells displaying TDP-43 nuclear mislocalization, with respect to cortical lesion area. In conclusion, we found no correlation between the percent of cortical NEUN positive cells displaying TDP-43 nuclear mislocalization with respect to the size of the cortical lesion area.