Mind Collage

I illustrate images that dive into different ideas but roughly stay around a few basic themes i\u27m drawn to. These themes link to either play with color theory, phycology, or images that take on a certain topics such as food, animals, nature, that mix together to create either an unusual narrative or a simple image. I prefer to create illustrations with ink pens, but I will also work with other materials such as pastels, charcoal, graphic and even digital mediums. Some of the inspirations for these works go back to artists Salvador dali and Rene Magritte. Both surrealists that painted strange images that narrate a story or emotion or an idea from their mind with interesting color pallet choices. This alone has always interested me for years. When an image pops into my head I want to do my best to draw it out for everyone to see. I\u27m not ashamed by my imagination but proud to express the creative thinking process I go through and adding my own personal meanings to them. Just goes to show how the mind wanders.https://digitalcommons.murraystate.edu/art399/1032/thumbnail.jp

Alzheimer's Disease Amyloid-β Links Lens and Brain Pathology in Down Syndrome

Down syndrome (DS, trisomy 21) is the most common chromosomal disorder and the leading genetic cause of intellectual disability in humans. In DS, triplication of chromosome 21 invariably includes the APP gene (21q21) encoding the Alzheimer's disease (AD) amyloid precursor protein (APP). Triplication of the APP gene accelerates APP expression leading to cerebral accumulation of APP-derived amyloid-β peptides (Aβ), early-onset AD neuropathology, and age-dependent cognitive sequelae. The DS phenotype complex also includes distinctive early-onset cerulean cataracts of unknown etiology. Previously, we reported increased Aβ accumulation, co-localizing amyloid pathology, and disease-linked supranuclear cataracts in the ocular lenses of subjects with AD. Here, we investigate the hypothesis that related AD-linked Aβ pathology underlies the distinctive lens phenotype associated with DS. Ophthalmological examinations of DS subjects were correlated with phenotypic, histochemical, and biochemical analyses of lenses obtained from DS, AD, and normal control subjects. Evaluation of DS lenses revealed a characteristic pattern of supranuclear opacification accompanied by accelerated supranuclear Aβ accumulation, co-localizing amyloid pathology, and fiber cell cytoplasmic Aβ aggregates (∼5 to 50 nm) identical to the lens pathology identified in AD. Peptide sequencing, immunoblot analysis, and ELISA confirmed the identity and increased accumulation of Aβ in DS lenses. Incubation of synthetic Aβ with human lens protein promoted protein aggregation, amyloid formation, and light scattering that recapitulated the molecular pathology and clinical features observed in DS lenses. These results establish the genetic etiology of the distinctive lens phenotype in DS and identify the molecular origin and pathogenic mechanism by which lens pathology is expressed in this common chromosomal disorder. Moreover, these findings confirm increased Aβ accumulation as a key pathogenic determinant linking lens and brain pathology in both DS and AD