Short communicationProgressive transformation of the cytoskeleton associated with normal aging and Alzheimer's disease☆
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SMI-32 labeling in Cajal-Retzius cells of feline primary visual cortex
2021, Neuroscience LettersCitation Excerpt :The Cajal-Retzius cells are extremely important for corticogenesis [3]. Whereas an expression of the HNF is a useful tool for the study for the pathogenesis of some neurological diseases like Alzheimer’s disease [24–27], Parkinson disease [28], lateral amyotrophic sclerosis [29], the HNF could be an interesting target for pathomorphological investigations related to study the corticogenesis deviations. Althoug, cat as a model are not so much common these days like it previously was, they still appear since that animal is much more suitable than rodents, for studying many phenomena for example, visual system development [30,15], locomotion and posture [31,32].
Combination treatment with leptin and pioglitazone in a mouse model of Alzheimer's disease
2017, Alzheimer's and Dementia: Translational Research and Clinical InterventionsAlterations in neurofilaments and the transformation of the cytoskeleton in axons may provide insight into the aberrant neuronal changes of Alzheimer's disease
2016, Brain Research BulletinCitation Excerpt :These ageing brain-related NFTs are predominantly intracellular and not linked to overt nerve cell death (Vickers et al., 1992a). This does likely make the cells particularly vulnerable to degeneration, as the entorhinal cortex also shows a relative abundance of ghost tangles at end-stage AD (Vickers et al., 1992a). With respect to end-stage AD, most NFTs in neocortical areas are still intracellular (Vickers et al., 1992a, 2003), further suggesting that tangle-related neurodegeneration is a slow process.
Neurofilament light gene deletion exacerbates amyloid, dystrophic neurite, and synaptic pathology in the APP/PS1 transgenic model of Alzheimer's disease
2015, Neurobiology of AgingCitation Excerpt :It lacks substantial tau pathology (Howlett et al., 2008) but demonstrates Aβ plaque–associated DNs with accumulations of NFs, α-internexin, synaptic proteins (Mitew et al., 2013b), and plaque-associated synapse loss (Mitew et al., 2013a). Notably, we were particularly interested in the effect of the diminution of NFs on DNs, as NF triplet–containing cortical neurons are selectively vulnerable to AD pathology (Hof and Morrison, 1991; Mitew et al., 2013b; Morrison et al., 1987; Vickers and Costa, 1992; Vickers et al., 1992b, 1994) and NF-containing DNs are the earliest neuronal change associated with Aβ plaque formation in the human brain (Dickson et al., 1999; Vickers et al., 1996). However, unexpectedly, our results showed that NFL deficiency in the APP/PS1 model increased neocortical neurite and synapse vulnerability to Aβ plaques and Aβ plaque pathology.
Life and Death of Neurons in The Aging Cerebral Cortex
2007, International Review of NeurobiologyCitation Excerpt :The association cortices are known to be involved in many aspects of cognition (Goldman‐Rakic, 1988). In AD, neurofilament protein–enriched neurons in certain neocortical and hippocampal areas are dramatically affected and die during NFT formation (Hof and Morrison, 1990, 2004; Hof et al., 1990; Morrison and Hof, 1997; Morrison et al., 1987; Vickers, 1997; Vickers et al., 1992, 1994, 2000). If the monkey data are considered within the context of the distribution of neurofilament protein–enriched neurons and NFTs in humans, it is likely that the human homologues of the neurofilament protein–enriched, corticocortically projecting neurons in the macaque monkey are those that are highly vulnerable in human AD.
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This work was funded by AG05138 and AG06647 from the National Institute for Aging and AHAF.
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We would like to thank our colleagues at the Fishberg Research Center for neurobiology as well as Dr. John Trojanowski and Dr. Neil Kowall for their valued comments on the manuscript. We also thank William Janssen for technical support and Bob Woolley for photographic assistance. In addition, we would like to acknowledge the Institute of Biogerontology Research Tissue Donation Program (Sun City, Arizona) for the provision of many of the cases in the present study.