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- Creators: Department of Psychology
- Member of: Barrett, The Honors College Thesis/Creative Project Collection
- Resource Type: Text
Does assisted cycle therapy influence activities of daily living in older adults with Down syndrome?
Alzheimer’s disease is a disease that can affect cognition, perception and behavior and is currently untreatable. It was discovered in the early 20th century and while significant scientific advancements have occurred, there is ambiguity that remains to be researched and understood. Latinos are the largest ethnic minority in the United States and while data still needs to be uncovered, possible risk factors for developing Alzheimer’s include heart issues, poverty and obesity, age and education level, to name a few. Poverty is linked to obesity, diabetes and a low education level, which in turn have been found to have an impact on Alzheimer’s and all factors impact cardiovascular and vascular health. Due to the collectivistic culture that is deeply rooted in Latinos, there is a strong sense of family that is upheld when caring for relatives who are afflicted and may be hesitant to receive the care that is needed. Other barriers include financial stability, linguistic and cultural barriers, underutilizing resources and health literacy. There are still research gaps that are yet to be filled like brain health and longitudinal studies for Latinos, but current treatments like diet and culturally competent professionals can help with the prognosis. Alzheimer’s is a complex disease, but with the numerous efforts made thus far, such as creating the LatinosAgainstAlzheimer’s Network, it will soon be able to be understood and hopefully eradicated.
Alzheimer’s disease (AD) is an irreversible brain disorder that plagues millions of people with no current cure. Current clinical research is slowly advancing to more definitive treatments in hopes of reducing the effects of progressive cognitive and behavioral decline, but none so far can slow AD’s onset. A brain area known as the nucleus incertus (NI) was recently discovered to potentially impact AD because of its connections to brain targets that degenerate; however, the NI’s role is unknown. This goal of this experiment was to use a transgenic mouse model (APP/PS1) that expresses AD pathology slowly as found in humans, and to test the mice in a variety of cognitive and anxiety assessments. Mice of both sexes and two different ages were used, with the first being young adult before AD pathology manifests (around 3-4 months old), and the second being around the cusp of when AD pathology manifests (late adult, 8-10 months old). The mice were tested in a variety of cognitive tasks that included the novel object recognition (NOR), Morris water maze (MWM), and the object placement (OP), with the latter being the focus of my thesis. Anxiety measures were taken from the open field (OF) and elevated plus maze (EPM) with the visible platform (VP) used to ensure mice could perform on the rigorous MWM task. In the OP, we found an age effect, where the older mice were less likely to explore the moved object during the OP compared to the younger mice; motor ability was unlikely to explain this effect. We did not find any significant age by genotype effects. These findings indicate that cognitive impairment only just started to affect the older cohort, since OP impairment was found on one measure and not another. Other measures currently being quantified will be helpful in understanding this data, and to see whether learning, memory, and anxiety are affected.
Alzheimer’s Disease (AD) is the most prevalent form of dementia and is the sixth leading cause of death in the elderly. Evidence suggests that forms of stress, including prenatal maternal stress (PMS), could exacerbate AD development. To better understand the mechanism linking PMS and AD, we investigated behavior and specific epigenetic markers of the 3xTg-AD mouse model compared to aged-controls in offspring of stressed mothers and non-stressed mothers.
Receptor-interacting serine/threonine protein kinase 1 (RIPK1) is an enzyme whose interaction with tumor necrosis factor receptor 1 (TNFR1) has been found to regulate cell death pathways, such as apoptosis and necroptosis, and neuroinflammation. Accumulating evidence in the past two decades has pointed to increased RIPK1 activity in various degenerative disorders, including Amyotrophic Lateral Sclerosis (ALS), stroke, traumatic brain injury (TBI) and Alzheimer’s Disease (AD). Given the work showing elevated RIPK1 in neurodegenerative disorders, to further understand the role of RIPK1 in disease pathogenesis, we created a conditional mouse overexpressing neuronal RIPK1 on a C57BL/6 background. These conditional transgenic mice overexpress murine RIPK1 under the CAMK2a neuronal promoter and the transgene is under the control of doxycycline. The removal of doxycycline turns on the RIPK1 transgene. Two cohorts of transgenic mice overexpressing neuronal RIPK1 (RIPK1 OE) were produced, and both had doxycycline removed at post-natal day 21. One cohort was behaviorally tested at 3-months-of-age and the second cohort was tested at 9-months-of-age. Behavioral testing included use of the RotaRod and the Morris water maze to assess motor coordination and spatial cognition, respectively. We found that the RIPK1 OE mice showed no deficits in motor coordination at either age but displayed spatial reference learning and memory deficits at 3- and 9-months-of-age. A subset of mice from two independent cohorts were utilized to assess RIPK1 levels and neuronal number. In these two cohorts of mice used for postmortem analysis, we found that at 3 months of age, ~2 months after transgene activation, RIPK1 levels are not higher in the hippocampus or cortex of the RIPK1 OE mice, however at 9 months, ~8 months after transgene activation, RIPK1 levels are significantly higher in the hippocampus and cortex of RIPK1 OE mice compared to the NonTg counterparts. A subset of tissue was stained against the neuronal marker NeuN. Using unbiased stereology to quantify hippocampal CA1 pyramidal neurons, we found no neuronal loss in the 3-month-old RIPK1 OE mice, but a 34.01% reduction in NeuN+ neuron count in 9-month-old RIPK1 OE mice. Collectively our data shows that RIPK1 overexpression impairs spatial reference learning and memory and reduces neuron number in the CA1 of the hippocampus, underlining the potential of RIPK1 as a target for ameliorating CNS pathology.