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Full-Text Articles in Neuroscience and Neurobiology
Analysis Of Chlamydia Pneumoniae And Ad-Like Pathology In The Brains Of Balb/C Mice Following Direct Intracranial Infection With Chlamydia Pneumoniae, Jessica Rachel Barton
Analysis Of Chlamydia Pneumoniae And Ad-Like Pathology In The Brains Of Balb/C Mice Following Direct Intracranial Infection With Chlamydia Pneumoniae, Jessica Rachel Barton
PCOM Biomedical Studies Student Scholarship
Alzheimer’s disease (AD) is an age-related progressive neurodegenerative disorder and the most common form of dementia. The pathology in the central nervous system (CNS) impairs memory and cognition, hindering the capabilities and the quality of life of the individual. This project continues studying the role of infection and Alzheimer’s disease and contributes to the overall understanding of the possible causes of this disease. In this study, BALB/c mice were infected, via direct intracranial injection, with a respiratory isolate (AR-39) of Chlamydia pneumoniae. Their brains were analyzed at 7 and 14 days post-infection, using immunohistochemistry, for the presence of C. …
Sirt1 Modulates Aggregation And Toxicity Through Deacetylation Of The Androgen Receptor In Cell Models Of Sbma, Heather L. Montie, Richard G. Pestell, Diane E. Merry
Sirt1 Modulates Aggregation And Toxicity Through Deacetylation Of The Androgen Receptor In Cell Models Of Sbma, Heather L. Montie, Richard G. Pestell, Diane E. Merry
PCOM Scholarly Papers
Posttranslational protein modifications can play a major role in disease pathogenesis; phosphorylation, sumoylation, and acetylation modulate the toxicity of a variety of proteotoxic proteins. The androgen receptor (AR) is substantially modified, in response to hormone binding, by phosphorylation, sumoylation, and acetylation; these modifications might thus contribute to DHT-dependent polyglutamine (polyQ)-expanded AR proteotoxicity in spinal and bulbar muscular atrophy (SBMA). SIRT1, a nuclear protein and deacetylase of the AR, is neuroprotective in many neurodegenerative disease models. Our studies reveal that SIRT1 also offers protection against polyQexpanded AR by deacetylating the AR at lysines 630/632/633. This finding suggested that nuclear AR acetylation …