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Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein
Transgenic mice that express high levels of human mutant APP support a primary role for APP/Aβ in the genesis of AD and could provide a preclinical model for testing therapeutic drugs.
Peripheral benzodiazepine receptors are colocalized with activated microglia following transient global forebrain ischemia in the rat
- D. Stephenson, D. Schober, E. Smalstig, RE Mincy, D. Gehlert, J. Clemens
- BiologyThe Journal of neuroscience : the official…
- 1 July 1995
The data strongly suggest that activated microglia rather than astrocytes express PBRs following ischemic insults, and lend further support to the application of 3H-PK11195 binding as a marker of neuronal injury in the brain.
Zyme, a Novel and Potentially Amyloidogenic Enzyme cDNA Isolated from Alzheimer’s Disease Brain*
- S. Little, E. Dixon, E. Johnstone
- Biology, ChemistryThe Journal of Biological Chemistry
- 3 October 1997
The discovery of a new serine protease from the AD brain by polymerase chain reaction amplification of DNA sequences representing active site homologous regions of chymotrypsin-like enzymes may indicate a role for this protease in amyloid precursor processing and AD.
Brain trauma induces massive hippocampal neuron death linked to a surge in beta-amyloid levels in mice overexpressing mutant amyloid precursor protein.
Cytosolic phospholipase A2 is induced in reactive glia following different forms of neurodegeneration
It is shown that in every condition evaluated, cytosolic phospholipase A2 is present in reactive glial cells within the precise region of neuron loss, and this results suggest that cytosol phospholips A2 may prove an attractive therapeutic target for neurodegeneration.
Transient Global Forebrain Ischemia Induces a Prolonged Expression of the Caspase-3 mRNA in Rat Hippocampal CA1 Pyramidal Neurons
The authors report that transient forebrain ischemia, which results in a delayed apoptotic death of CA1 pyramidal neurons, results in prolonged expression of caspase-3 mRNA in these same pyramid neurons, and suggests that transcriptional activation of this casp enzyme-3 gene may be involved in the apoptotic cell death cascade ofCA1 neurons after transient global ischemIA.
Transcription Factor Nuclear Factor-Kappa B is Activated in Neurons after Focal Cerebral Ischemia
It is demonstrated that transient focal cerebral ischemia results in activation ofNF-kB in neurons and supports previous observations that neuroprotective antioxidants may inhibit neuronal death by preventing the activation of NF-kB.
Brain Trauma in Aged Transgenic Mice Induces Regression of Established Aβ Deposits
Previously accumulated Abeta plaques resulting from progressive amyloidosis in the AD brain also may be reversible, and these data suggest that previously accumulated Abetas plaque burden in the hippocampus ipsilateral to TBI is reversible.
Traumatic brain injury in young, amyloid-beta peptide overexpressing transgenic mice induces marked ipsilateral hippocampal atrophy and diminished Abeta deposition during aging.
The data suggest that the vulnerability of brain cells to Abeta toxicity increases and that the accumulation of Abeta deposits decrease in the penumbra of CCI months after TBI, which is relevant for investigating the poorly understood role that TBI and other epigenetic risk factors play in the onset and/or progression of AD.