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Articles 1 - 5 of 5
Full-Text Articles in Neuroscience and Neurobiology
Meox2 Haploinsufficiency Increases Neuronal Cell Loss In A Mouse Model Of Alzheimer's Disease, Ileana Soto Reyes, Weronika A. Grabowska, Kristen D. Onos, Leah C. Graham, Harriet M. Jackson, Stephen N. Simeone, Gareth R. Howell
Meox2 Haploinsufficiency Increases Neuronal Cell Loss In A Mouse Model Of Alzheimer's Disease, Ileana Soto Reyes, Weronika A. Grabowska, Kristen D. Onos, Leah C. Graham, Harriet M. Jackson, Stephen N. Simeone, Gareth R. Howell
Ileana Soto Reyes
Evidence suggests that multiple genetic and environmental factors conspire together to increase susceptibility to Alzheimer's disease (AD). The amyloid cascade hypothesis states that deposition of the amyloid-β (Aβ) peptide is central to AD; however, evidence in humans and animals suggests that Aβ buildup alone is not sufficient to cause neuronal cell loss and cognitive decline. Mouse models that express high levels of mutant forms of amyloid precursor protein and/or cleaving enzymes deposit amyloid but do not show neuron loss. Therefore, a double-hit hypothesis for AD has been proposed whereby vascular dysfunction precedes and promotes Aβ toxicity. In support of this, …
Deficiency Of Complement Component 5 Ameliorates Glaucoma In Dba/2j Mice, Gareth R. Howell, Ileana Soto Reyes, Margaret Ryan, Leah C. Graham, Richard S. Smith, Simon W.M. John
Deficiency Of Complement Component 5 Ameliorates Glaucoma In Dba/2j Mice, Gareth R. Howell, Ileana Soto Reyes, Margaret Ryan, Leah C. Graham, Richard S. Smith, Simon W.M. John
Ileana Soto Reyes
Background Glaucoma is an age-related neurodegenerative disorder involving the loss of retinal ganglion cells (RGCs), which results in blindness. Studies in animal models have shown that activation of inflammatory processes occurs early in the disease. In particular, the complement cascade is activated very early in DBA/2J mice, a widely used mouse model of glaucoma. A comprehensive analysis of the role of the complement cascade in DBA/2J glaucoma has not been possible because DBA/2J mice are naturally deficient in complement component 5 (C5, also known as hemolytic complement, Hc), a key mediator of the downstream processes of the complement cascade, including …
Chronic Consumption Of A Western Diet Induces Robust Glial Activation In Aging Mice And In A Mouse Model Of Alzheimer’S Disease, Leah C. Graham, Jeffrey M. Harder, Ileana Soto Reyes, Wilhelmine N. De Vries, Simon W. M. John, Gareth R. Howell
Chronic Consumption Of A Western Diet Induces Robust Glial Activation In Aging Mice And In A Mouse Model Of Alzheimer’S Disease, Leah C. Graham, Jeffrey M. Harder, Ileana Soto Reyes, Wilhelmine N. De Vries, Simon W. M. John, Gareth R. Howell
Ileana Soto Reyes
Studies have assessed individual components of a western diet, but no study has assessed the long-term, cumulative effects of a western diet on aging and Alzheimer’s disease (AD). Therefore, we have formulated the first western-style diet that mimics the fat, carbohydrate, protein, vitamin and mineral levels of western diets. This diet was fed to aging C57BL/6J (B6) mice to identify phenotypes that may increase susceptibility to AD, and to APP/PS1 mice, a mouse model of AD, to determine the effects of the diet in AD. Astrocytosis and microglia/monocyte activation were dramatically increased in response to diet and was further increased …
Dba/2j Mice Are Susceptible To Diabetic Nephropathy And Diabetic Exacerbation Of Iop Elevation, Ileana Soto Reyes, Gareth R. Howell, Cai W. John, Joseph L. Kief, Richard T. Libby, Simon W.M. John
Dba/2j Mice Are Susceptible To Diabetic Nephropathy And Diabetic Exacerbation Of Iop Elevation, Ileana Soto Reyes, Gareth R. Howell, Cai W. John, Joseph L. Kief, Richard T. Libby, Simon W.M. John
Ileana Soto Reyes
Some pathological manifestations of diabetes in the eye include retinopathy, cataracts and elevated intraocular pressure (IOP). Loss of retinal ganglion cells (RGCs) in non-proliferative stages of diabetic retinopathy and small increases in IOP in diabetic patients has raised the possibility that diabetes affects the development and progression of ocular hypertension and glaucoma. The Ins2Akita mutation is known to cause diabetes and retinopathy on a C57BL/6J (B6) background by as early as 3 months of age. Here, the impact of the Akita mutation on glaucoma was assessed using DBA/2J (D2) mice, a widely used mouse model of ocular hypertension induced glaucoma. …
Apoe Stabilization By Exercise Prevents Aging Neurovascular Dysfunction And Complement Induction, Ileana Soto Reyes, Leah C. Graham, Hannah J. Richter, Stephen N. Simeone, Jake E. Radell, Weronika Grabowska, W. Keith Funkhouser, Megan C. Howell, Gareth R. Howell
Apoe Stabilization By Exercise Prevents Aging Neurovascular Dysfunction And Complement Induction, Ileana Soto Reyes, Leah C. Graham, Hannah J. Richter, Stephen N. Simeone, Jake E. Radell, Weronika Grabowska, W. Keith Funkhouser, Megan C. Howell, Gareth R. Howell
Ileana Soto Reyes
Aging is the major risk factor for neurodegenerative diseases such as Alzheimer's disease, but little is known about the processes that lead to age-related decline of brain structures and function. Here we use RNA-seq in combination with high resolution histological analyses to show that aging leads to a significant deterioration of neurovascular structures including basement membrane reduction, pericyte loss, and astrocyte dysfunction. Neurovascular decline was sufficient to cause vascular leakage and correlated strongly with an increase in neuroinflammation including up-regulation of complement component C1QA in microglia/monocytes. Importantly, long-term aerobic exercise from midlife to old age prevented this age-related neurovascular decline, …