Please use this identifier to cite or link to this item: https://doi.org/10.1002/glia.20218
Title: Temporal profiles of neuronal degeneration, glial proliferation, and cell death in hNFL(+/+) and NFL(-/-)mice
Authors: McLean, J.R.
Sanelli, T.R.
Leystra-Lantz, C.
He, B.P. 
Strong, M.J.
Keywords: ALS
Apoptosis
Astrocytes
Heat shock protein
Microglia
Neurofilament
Protein aggregates
Issue Date: Oct-2005
Citation: McLean, J.R., Sanelli, T.R., Leystra-Lantz, C., He, B.P., Strong, M.J. (2005-10). Temporal profiles of neuronal degeneration, glial proliferation, and cell death in hNFL(+/+) and NFL(-/-)mice. GLIA 52 (1) : 59-69. ScholarBank@NUS Repository. https://doi.org/10.1002/glia.20218
Abstract: Neurofilament (NF) aggregate formation within motor neurons is a pathological hallmark of both the sporadic and familial forms of amyotrophic lateral sclerosis (ALS). The relationship between aggregate formation and both microglial and astrocytic proliferation, as well as additional neuropathological features of ALS, is unknown. To examine this, we have used transgenic mice that develop NF aggregates, through either a lack of the low-molecular-weight NF subunit [NFL (-/-)] or the overexpression of human NFL [hNFL (+/+)]. Transgenic and wild-type C57bl/6 mice were examined from 1 month to 18 months of age, and the temporal pattern of motor neuron degeneration, microglial and astrocytic proliferation, and heat shock protein-70 (HSP-70) expression characterized. We observed three overlapping phases in both transgenic mice, including transient aggregate formation, reactive microgliosis, and progressive motor neuron loss. However, only NFL (-/-) mice demonstrated significant astrogliosis and HSP-70 upregulation in both motor neurons and astrocytes. These in vivo models suggest that the development of NF aggregates in motor neurons leads to motor neuron death, but that the interaction between the degenerating motor neurons and the adjacent non-neuronal cells may differ significantly depending on the etiology of the NF aggregate itself. ©2005 Wiley-Liss, Inc.
Source Title: GLIA
URI: http://scholarbank.nus.edu.sg/handle/10635/120686
ISSN: 08941491
DOI: 10.1002/glia.20218
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