2015
DOI: 10.1016/j.neurobiolaging.2015.07.003
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Neurofilament light gene deletion exacerbates amyloid, dystrophic neurite, and synaptic pathology in the APP/PS1 transgenic model of Alzheimer's disease

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Cited by 29 publications
(37 citation statements)
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“…Therefore, TRIM2 seemed to play crucial roles in this modulating process. However, it is reported that mutation or loss of function of TRIM2 will lead to the accumulation of NF-L resulting in progressive neurodegeneration [19,27], while NF-L deficiency significantly increases neocortical dystrophic neuritis pathology and Aβ deposition as well as synapse vulnerability [46]. Therefore, maintaining expressive balance of TRIM2 is important.…”
Section: Discussionmentioning
confidence: 99%
“…Therefore, TRIM2 seemed to play crucial roles in this modulating process. However, it is reported that mutation or loss of function of TRIM2 will lead to the accumulation of NF-L resulting in progressive neurodegeneration [19,27], while NF-L deficiency significantly increases neocortical dystrophic neuritis pathology and Aβ deposition as well as synapse vulnerability [46]. Therefore, maintaining expressive balance of TRIM2 is important.…”
Section: Discussionmentioning
confidence: 99%
“…Previous studies have used this experimental approach to investigate the role of NFs in different transgenic mouse models of neurodegenerative disease however, the resulting phenotype alterations have been disparate [32,33]. Interestingly, tau transgenic mice (T44) showed a delay in disease onset [33] whereas APP/PS1 transgenic mice displayed increased levels of pathology and synaptic vulnerability when NFL was absent [32]. In the present study, we observed no major differences in the onset of disease or αS pathology in human A53T αS transgenic (M83) mice [40] with or without NFL following αS fibril seeding from intramuscular injection.…”
Section: Discussionmentioning
confidence: 99%
“…The involvement of NFs in neurodegeneration is an active area of research and has been investigated by breeding transgenic mouse models of AD and tauopathy onto an NFL null background in order to assess the contribution of NFs to the pathogenesis of disease in these particular models [32,33]. Ishihara and colleagues observed delayed development of the typical behavioral phenotype and reduced pathology in mice transgenic for human tau (T44 mice)[34] when they lacked NFs compared toT44 mice with NFs [33] suggesting that NFs, at least in part, contribute to the onset of tauopathy in these mice.…”
Section: Introduction1mentioning
confidence: 99%
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