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Volume 16, Number 18, Issue of September 15, 1996 pp. 5795-5811
Copyright ©1996 Society for Neuroscience

Comparison of Neurodegenerative Pathology in Transgenic Mice Overexpressing V717F beta -Amyloid Precursor Protein and Alzheimer's Disease

Received Jan. 11, 1996; revised June 19, 1996; accepted July 3, 1996.

Eliezer Masliah1, 2, Abbyann Sisk1, Margaret Mallory1, Lennart Mucke3, Dale Schenk4, and Dora Games4

Departments of 1 Neurosciences and 2 Pathology, University of California-San Diego, La Jolla, California 92093-0624, 3 Molecular Neurobiology Program, The Gladstone Institute, San Francisco, California 94141-9100, and 4 Athena Neurosciences, Inc., South San Francisco, California 94080

Overexpression of mutated human amyloid precursor protein (hAPP717Vright-arrowF) under control of platelet-derived growth factor promoter (PDAPP minigene) in transgenic (tg) mice results in neurodegenerative changes similar to Alzheimer's disease (AD). To clarify the pathology of these mice, we studied images derived from laser scanning confocal and electron microscopy and performed comparisons between PDAPP tg mice and AD. Similar to AD, neuritic plaques in PDAPP tg mouse contained a dense amyloid core surrounded by anti-hAPP- and anti-neurofilament-immunoreactive dystrophic neurites and astroglial cells. Neurons were found in close proximity to plaques in PDAPP tg mice and, to a lesser extent, in AD. In PDAPP tg mice, and occasionally in AD, neuronal processes contained fine intracellular amyloid fibrils in close proximity to the rough endoplasmic reticulum, coated vesicles, and electron-dense material. Extracellular amyloid fibrils (9-11 nm in diameter) were abundant in PDAPP tg and were strikingly similar to those observed in AD. Dystrophic neurites in plaques of PDAPP tg mouse and AD formed synapses and contained many dense multilaminar bodies and neurofilaments (10 nm). Apoptotic-like figures were present in the tg mice. No paired helical filaments have yet been observed in the heterozygote PDAPP tg mice. In summary, this study shows that PDAPP tg mice develop massive neuritic plaque formation and neuronal degeneration similar to AD. These findings show that overproduction of hAPP717Vright-arrowF in tg mice is sufficient to cause not only amyloid deposition, but also many of the complex subcellular degenerative changes associated with AD.

Key words: Alzheimer's disease; amyloid precursor protein; transgenic; electron microscopy; confocal microscopy; neurodegeneration




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J. H. Morrison and P. R. Hof
Life and Death of Neurons in the Aging Brain
Science, October 17, 1997; 278(5337): 412 - 419.
[Abstract] [Full Text]