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Honors Theses

Permanent URI for this collectionhttps://hdl.handle.net/10217/240488

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    The multitude of aphantasia subtypes and their respective cognitive differences and pathological considerations: a review on the merging condition
    (Colorado State University. Libraries, 2024) White, Makenna, author
    Aphantasia is an emerging condition defined as the lack or absence of voluntary imagery. However, there are wide-ranging individual cognitive profiles due to the condition's heterogeneity. While the metacognition and sensory imagery deficit debate has been resolved in favor of the sensory imagery deficit theory due to the correlation of behavioral correlations with objective measures there is still much debate over the general nature of the condition. Much of this confusion arises from the multitude of subtypes and the complicated nature of mental imagery pathways. Aphantasia as a condition is complicated by the fact that it can be acquired and congenital with congenital aphantasia being made up of many different subtypes. While visual aphantasia, a lack of visual mental imagery, is the most prominently studied type there are also multisensory, deficits in all sense modalities, and combinatorial, deficits in two or more sense modalities. The prevalence of these subtypes makes it more difficult to determine distinct etiologies and a common cognitive profile. Despite this, there are new emerging cognitive theories based on the reverse hierarchy model and scene construction theory attempting to further understanding of the condition. The most comprehensive area of aphantasia study is the cognitive profile which generally shows intact perception, intact abilities on tasks thought to rely on mental imagery, and some deficits in memory, dreaming, and emotional processing. Mixed dreaming evidence in aphantasia research has also led to a debate about whether the condition impacts involuntary imagery in the same way it impacts voluntary imagery though this evidence is unclear. However, some of the emotional processing deficits lead to questions about mental health diagnostics and treatment. Overall, aphantasia as a whole has an overall lack of general research definition and diagnosis leading to conflicting research results. The lack of subtype separation adds to this complication.
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    The rotenone exposure model of Parkinson's disease induces progressive locomotor deficits in mice
    (Colorado State University. Libraries, 2024-12-06) Yates, Nicole E., author
    Neurodegenerative diseases remain the leading cause of physical and cognitive disability worldwide. Within this group of diseases, Parkinson's disease (PD) is the second most common age-related neurodegenerative disorder affecting an estimated 9.4 million people worldwide in 2020. It is characterized by the selective degeneration of dopaminergic neurons (DAn) in the substantia nigra pars compacta (SNpc), increased glial activation, and inflammatory signaling. Clinical motor symptoms include resting tremor, hunched posture, difficulties initiating movement, and a short shuffling gait. Exposure to environmental neurotoxins such as pesticides can recapitulate key pathological features of PD. Among such agents is the naturally occurring pesticide, rotenone, a mitochondrial complex I uncoupler that targets DAn in the SNpc, leading to parkinsonian phenotype in rodent models. However, it remains unknown how this toxin elicits gait disturbances throughout the course of exposure. In this study, inbred C57Bl/6 mice were exposed to 2.5 mg/kg/day of rotenone or respective vehicle control for 14 days, followed by a 7 day lesioning period. Using the Noldus CatWalk XT, a high-throughput gait tracking and analysis system, alterations in gait and locomotion were examined over the course of rotenone exposure and subsequent lesioning period. The resulting data demonstrates that rotenone exposure alters locomotion by decreasing stride lengths and speed of movements both in individual paws and with the animal's gait as a whole. The exposure induced changes in animals that progressed even after the cessation of exposure. This suggests that rotenone-induced neurotoxicity causes a sustained response in the brain leading to progressive neurologic and motor dysfunction, similar to that observed in patients with idiopathic PD.