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Volume 17, Number 18, Issue of September 15, 1997 pp. 7053-7059
Copyright ©1997 Society for Neuroscience

Abeta Deposition Is Associated with Neuropil Changes, but not with Overt Neuronal Loss in the Human Amyloid Precursor Protein V717F (PDAPP) Transgenic Mouse

Received April 4, 1997; revised June 4, 1997; accepted July 1, 1997.

Michael C. Irizarry1, Ferdie Soriano2, Megan McNamara1, Keith J. Page1, Dale Schenk2, Dora Games2, and Bradley T. Hyman1

1 Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, 02114 and 2 Athena Neurosciences, South San Francisco, California 94080

The PDAPP transgenic mouse overexpresses human amyloid precursor protein V717F (PDAPP minigene) and develops age-related cerebral amyloid-beta protein (Abeta ) deposits similar to senile plaques in Alzheimer's disease. We find age-related cortical and limbic Abeta deposition that begins at 8 months and progresses to cover 20-50% of the neuropil in cingulate cortex, entorhinal cortex, and hippocampus of 18-month-old heterozygotic animals. The regional patterns of transgene expression and amyloid deposition suggest that Abeta deposits occur at the terminals of overexpressing neurons. Amyloid deposition is associated with dystrophic neurites and extensive gliosis. However, stereological analysis shows that there is no overt neuronal loss in entorhinal cortex, CA1 hippocampal subfield, or cingulate cortex through 18 months of age. In addition, there is no apparent loss of mRNA encoding neuronal synaptic, cytoskeletal, or metabolic proteins. Thus, widespread Abeta deposition in 18-month-old heterozygotic mice produces neuritic alterations and gliosis without widespread neuronal death.

Key words: transgenic mice; Alzheimer's disease; hippocampus; amyloid; amyloid precursor protein; cingulate cortex; entorhinal cortex; neuritic dystrophy; synaptophysin; microtubule associated protein-2; cytochrome oxidase; glial fibrillary acidic protein




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