Developing A Mouse Model Of Sporadic Alzheimer s Disease

Developing A Mouse Model Of Sporadic Alzheimer’s Disease By Invoking The Systemic Immune Response Using Polyriboinosinic-Polyribocytidilic Acid (PolyI:C) Sahar Salimi-Mosavi, Human Biology Program, University of Toronto, Dr. Lili-Naz Hazrati, Department of Laboratory of Medicine and Pathology, Tanz Centre for Research in Neurodegenerative Diseases Turnitin receipt #: 549076367 Abstract Alzheimer’s disease (AD) is one of the most widespread forms of dementia in the aging population. Unfortunately, most cases of AD are sporadic in nature and the underlying etiology is unknown. Thus far, the majority of the experiments have been based on transgenic mice models where amyloid aggregations are the causal initiator of AD. However, recent evidence has suggested that chronic inflammation may precede the induction of late-onset AD neuropathology. To demonstrate the role of neuroinflamamtion in late-onset development of AD, we injected a viral mimic polyinosinic:polycytidylic acid (polyI:C) to C57BL/6J pregnant mice during gestational day 17 (GD17). A subset of the pups were exposed to a second injection at 12 months of age to observe whether a second immune challenge would increase the rate of AD development. The aged mice were subjected to a cued fear-conditioning task to measure their cognitive capacity, and immunoblotting and immunohistochemistry to detect any neu ropathological changes. PolyI:C injected mice failed to show any significant cognitive impairments following theirShow MoreRelatedExplain the Difference Between Mendelian and Non-Mendelian Diseases. Using One Neuropsychiatric Disorder (Schizophrenia) Discuss the Progress Made so Far in Understanding the Genetic Architecture of That Disorder5164 Words   |  21 Pagesdiscussion of the Progress made so far in understanding the Genetic Architecture of Schizophrenia Schizophrenia: An Elusive Complex Disorder A discussion of the Progress made so far in understanding the Genetic Architecture of Schizophrenia Mendelian diseases conform to Mendel’s laws of genetic inheritance; segregation and independent assortment. Therefore, every pair of alleles in diploid organisms, are separated during meiosis and one allele for every trait is passed onto one of the two daughter cells