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Detection Of Bacterial Antigens And Alzheimer's Disease-Like Pathology In The Central Nervous System Of Balb/C Mice Following Intranasal Infection With A Laboratory Isolate Of Chlamydia Pneumoniae, C. Scott Little Phd, Timothy A. Joyce, Christine Hammond, Hazem Matta, David Cahn, Denah Appelt, Brian J. Balin Phd
Detection Of Bacterial Antigens And Alzheimer's Disease-Like Pathology In The Central Nervous System Of Balb/C Mice Following Intranasal Infection With A Laboratory Isolate Of Chlamydia Pneumoniae, C. Scott Little Phd, Timothy A. Joyce, Christine Hammond, Hazem Matta, David Cahn, Denah Appelt, Brian J. Balin Phd
PCOM Scholarly Papers
Pathology consistent with that observed in Alzheimer’s disease (AD) has previously been documented following intranasal infection of normal wild-type mice with Chlamydia pneumoniae (Cpn) isolated from an AD brain (96-41). In the current study, BALB/c mice were intranasally infected with a laboratory strain of Cpn, AR-39, and brain and olfactory bulbs were obtained at 1-4 months post-infection (pi). Immunohistochemistry for amyloid beta or Cpn antigens was performed on sections from brains of infected or mock-infected mice. Chlamydia-specific immunolabeling was identified in olfactory bulb tissues and in cerebrum of AR-39 infected mice. The Cpn specific labeling was most prominent at 1 …
Phenotype Of Transgenic Mice Carrying A Very Low Copy Number Of The Mutant Human G93a Superoxide Dismutase-1 Gene Associated With Amyotrophic Lateral Sclerosis, Jeffrey S. Deitch, Guillermo M. Alexander, Andrew Bensinger, Steven Yang, Juliann T. Jiang, Terry D. Heiman-Patterson
Phenotype Of Transgenic Mice Carrying A Very Low Copy Number Of The Mutant Human G93a Superoxide Dismutase-1 Gene Associated With Amyotrophic Lateral Sclerosis, Jeffrey S. Deitch, Guillermo M. Alexander, Andrew Bensinger, Steven Yang, Juliann T. Jiang, Terry D. Heiman-Patterson
PCOM Scholarly Papers
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease of the motor neuron. While most cases of ALS are sporadic, 10% are familial (FALS) with 20% of FALS caused by a mutation in the gene that codes for the enzyme Cu/Zn superoxide dismutase (SOD1). There is variability in sporadic ALS as well as FALS where even within the same family some siblings with the same mutation do not manifest disease. A transgenic (Tg) mouse model of FALS containing 25 copies of the mutant human SOD1 gene demonstrates motor neuron pathology and progressive weakness similar to ALS patients, leading to death …