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Age-associated and cell-type-specific neurofibrillary pathology in transgenic mice expressing the human midsized neurofilament subunit

JC Vickers, JH Morrison, VL Friedrich Jr, GA Elder, DP Perl, RN Katz and RA Lazzarini
Journal of Neuroscience 1 September 1994, 14 (9) 5603-5612; DOI: https://doi.org/10.1523/JNEUROSCI.14-09-05603.1994
JC Vickers
Fishberg Research Center for Neurobiology, Mount Sinai School of Medicine, New York, New York 10029–6574.
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JH Morrison
Fishberg Research Center for Neurobiology, Mount Sinai School of Medicine, New York, New York 10029–6574.
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VL Friedrich Jr
Fishberg Research Center for Neurobiology, Mount Sinai School of Medicine, New York, New York 10029–6574.
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GA Elder
Fishberg Research Center for Neurobiology, Mount Sinai School of Medicine, New York, New York 10029–6574.
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DP Perl
Fishberg Research Center for Neurobiology, Mount Sinai School of Medicine, New York, New York 10029–6574.
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RN Katz
Fishberg Research Center for Neurobiology, Mount Sinai School of Medicine, New York, New York 10029–6574.
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RA Lazzarini
Fishberg Research Center for Neurobiology, Mount Sinai School of Medicine, New York, New York 10029–6574.
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Abstract

Alterations in neurofilaments are a common occurrence in neurons of the human nervous system during aging and diseases associated with aging. Such pathologic changes may be attributed to species-specific properties of human neurofilaments as well as cell-type-specific regulation of this element of the cytoskeleton. The development of transgenic animals containing human neurofilament subunits offers an opportunity to study the effects of aging and other experimental conditions on the human-specific form of these proteins in a rodent model. The present study shows that mice from the transgenic line NF(M)27, which express the human midsized neurofilament subunit at low levels (2–25% of the endogenous NF-M), develop neurofilamentous accumulations in specific subgroups of neurons that are age dependent, affecting 78% of transgenic mice over 12 months of age. Similar accumulations do not occur in age-matched, wild-type littermates or in 3-month-old transgenic mice. In 12-month-old transgenic mice, somatic neurofilament accumulations resembling neurofibrillary tangles were present predominantly in layers III and V of the neocortex, as well as in select subpopulations of subcortical neurons. Intraperikaryal, spherical neurofilamentous accumulations were particularly abundant in cell bodies in layer II of the neocortex, and neurofilament-containing distentions of Purkinje cell proximal axons occurred in the cerebellum. These pathological accumulations contained mouse as well as human NF subunits, but could be distinguished by their content of phosphorylation-dependent NF epitopes. These cytoskeletal alterations closely resemble the cell-type-specific alterations in neurofilaments that occur during normal human aging and in diseases associated with aging, indicating that these transgenic animals may serve as models of some aspects of the pathologic features of human neurodegenerative diseases.

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The Journal of Neuroscience: 14 (9)
Journal of Neuroscience
Vol. 14, Issue 9
1 Sep 1994
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Age-associated and cell-type-specific neurofibrillary pathology in transgenic mice expressing the human midsized neurofilament subunit
JC Vickers, JH Morrison, VL Friedrich Jr, GA Elder, DP Perl, RN Katz, RA Lazzarini
Journal of Neuroscience 1 September 1994, 14 (9) 5603-5612; DOI: 10.1523/JNEUROSCI.14-09-05603.1994

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Age-associated and cell-type-specific neurofibrillary pathology in transgenic mice expressing the human midsized neurofilament subunit
JC Vickers, JH Morrison, VL Friedrich Jr, GA Elder, DP Perl, RN Katz, RA Lazzarini
Journal of Neuroscience 1 September 1994, 14 (9) 5603-5612; DOI: 10.1523/JNEUROSCI.14-09-05603.1994
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