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Full-Text Articles in Neuroscience and Neurobiology
Potential And Limitations Of Using Stem Cells To Cure Alzheimer’S Disease: A Literature Review Of Its Potential And Ethical Limitations In Translation To Human Trials, Eleni Zivla
OUR Journal: ODU Undergraduate Research Journal
Alzheimer's disease has become one of the most significant, life-limiting illnesses of our time as a result of the rapid increase in the average life expectancy. To successfully develop a cure for this yet incurable disease, one must understand the pathology of Alzheimer’s disease. As found in recent research studies, a brain that is diagnosed with Alzheimer's is characterized by the presence of extracellular amyloid plaques composed of the amyloid-beta (Aβ) peptide and intracellular neurofibrillary tangles composed of the microtubule-associated protein: tau. In this literature review, several stem cell therapies are being reviewed as a potential cure for Alzheimer’s disease …
Left Lateralized Cerebral Glucose Metabolism Declines In Amyloid-Β Positive Persons With Mild Cognitive Impairment, Christopher M. Weise, Kewei Chen, Yinghua Chen, Xiaoying Kuang, Cary R. Savage, Eric M. Reiman
Left Lateralized Cerebral Glucose Metabolism Declines In Amyloid-Β Positive Persons With Mild Cognitive Impairment, Christopher M. Weise, Kewei Chen, Yinghua Chen, Xiaoying Kuang, Cary R. Savage, Eric M. Reiman
Center for Brain, Biology, and Behavior: Faculty and Staff Publications
Background: Previous publications indicate that Alzheimer's Disease (AD) related cortical atrophy may develop in asymmetric patterns, with accentuation of the left hemisphere. Since fluorodeoxyglucose positron emission tomography (FDG PET) measurements of the regional cerebral metabolic rate of glucose (rCMRgl) provide a sensitive and specific marker of neurodegenerative disease progression, we sought to investigate the longitudinal pattern of rCMRgl in amyloid-positive persons with mild cognitive impairment (MCI) and dementia, hypothesizing asymmetric declines of cerebral glucose metabolism. Methods: Using florbetapir PET and cerebrospinal fluid (CSF) measures to define amyloid-β (Aβ) positivity, 40 Aβ negative (Aβ-) cognitively unimpaired controls (CU; 76 ± 5y), …
Investigating The Pathological Response To Beta Amyloid Toxicity In Rats: The Role Of Age And The Antioxidant Catalase-Skl, Hayley J. Nell
Investigating The Pathological Response To Beta Amyloid Toxicity In Rats: The Role Of Age And The Antioxidant Catalase-Skl, Hayley J. Nell
Electronic Thesis and Dissertation Repository
Accumulation of beta-amyloid (Aβ) in the brain is a major contributor to the cellular pathology and cognitive impairment observed in Alzheimer’s disease (AD). In part, Aβ exerts its toxic effects by increasing reactive oxygen species (ROS) and neuroinflammation in the brain. Aging, a major risk factor for AD is also associated with increased production of ROS. This study investigated the age-related pathological response to Aβ toxicity and examined whether catalase-SKL(CAT-SKL), a genetically engineered derivative of the peroxisomal antioxidant enzyme catalase, is able to reduce Aβ toxicity. Bilateral intracerebroventricular (icv) injections of the Aβ25-35 peptide was used to model Aβ …
An Investigation Into The Combined Effects Of Β-Amyloid Toxicity And Cerebral Ischemia On The Pathological Expression Of Gangliosides., Jeffrey D. Hepburn
An Investigation Into The Combined Effects Of Β-Amyloid Toxicity And Cerebral Ischemia On The Pathological Expression Of Gangliosides., Jeffrey D. Hepburn
Electronic Thesis and Dissertation Repository
Identifying mechanisms underlying the synergistic pathological interaction between stroke and Alzheimer’s disease (AD) can effectively guide future therapeutic strategies for these highly co-morbid conditions. Aberrant ganglioside expression marked by the pathological accumulation of ganglioside GM3 is common to stroke and AD, yet it is unclear whether GM3 is synergistically enhanced in a comorbid model, or if GM3 is a viable therapeutic target. Adult male Wistar rats received a unilateral ischemic striatal infarct via endothelin-1 (ET-1) injection alone or in combination with bilateral intracerebroventricular injection of the β-Amyloid 25-35 peptide (Aβ) to induce generalized Aβ toxicity (Aβ/ET-1). Animals were sacrificed after …