Increased sensory neuron apoptotic death 2 weeks after peripheral axotomy in C57BL/6J mice compared to A/J mice

Pierucci, Amauri; Oliveira, Alexandre Leite Rodrigues de

doi:10.1016/j.neulet.2005.11.024

Cited by 10 publications

(6 citation statements)

References 32 publications

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“…Pathological changes in the upper cortex could be associated with degeneration of the feedforward cortico‐cortical projections, which have their cells or origin in laminae II/III as shown in other disorders [16]. By contrast, EN, which may reflect either a stress response [58,59] or axonal degeneration [60,61], and glial cell nuclei were more abundant in the lower cortex consistent with degeneration of the lower laminae in FTLD‐TDP. Pathological changes in lower cortex could result from degeneration of either the feedback cortico‐cortical projections [16] or the afferent and efferent cortical‐subcortical projections.…”

Section: Discussionmentioning

confidence: 83%

Laminar distribution of the pathological changes in sporadic frontotemporal lobar degeneration with transactive response (TAR) DNA‐binding protein of 43 kDa (TDP‐43) proteinopathy: a quantitative study using polynomial curve fitting

Armstrong

Hamilton

Hedreen

et al. 2013

Neuropathology Appl Neurobio

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R. A. Armstrong, R. L. Hamilton, I. R. A. Mackenzie, J. Hedreen and N. J. Cairns (2013) Neuropathology and Applied Neurobiology39, 335–347 Laminar distribution of the pathological changes in sporadic frontotemporal lobar degeneration with transactive response (TAR) DNA‐binding protein of 43 kDa (TDP‐43) proteinopathy: a quantitative study using polynomial curve fitting Aims: Previous data suggest heterogeneity in laminar distribution of the pathology in the molecular disorder frontotemporal lobar degeneration (FTLD) with transactive response (TAR) DNA‐binding protein of 43 kDa (TDP‐43) proteinopathy (FTLD‐TDP). To study this heterogeneity, we quantified the changes in density across the cortical laminae of neuronal cytoplasmic inclusions, glial inclusions, neuronal intranuclear inclusions, dystrophic neurites, surviving neurones, abnormally enlarged neurones, and vacuoles in regions of the frontal and temporal lobe. Methods: Changes in density of histological features across cortical gyri were studied in 10 sporadic cases of FTLD‐TDP using quantitative methods and polynomial curve fitting. Results: Our data suggest that laminar neuropathology in sporadic FTLD‐TDP is highly variable. Most commonly, neuronal cytoplasmic inclusions, dystrophic neurites and vacuolation were abundant in the upper laminae and glial inclusions, neuronal intranuclear inclusions, abnormally enlarged neurones, and glial cell nuclei in the lower laminae. TDP‐43‐immunoreactive inclusions affected more of the cortical profile in longer duration cases; their distribution varied with disease subtype, but was unrelated to Braak tangle score. Different TDP‐43‐immunoreactive inclusions were not spatially correlated. Conclusions: Laminar distribution of pathological features in 10 sporadic cases of FTLD‐TDP is heterogeneous and may be accounted for, in part, by disease subtype and disease duration. In addition, the feedforward and feedback cortico‐cortical connections may be compromised in FTLD‐TDP.

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Section: Discussionmentioning

confidence: 83%

Laminar distribution of the pathological changes in sporadic frontotemporal lobar degeneration with transactive response (TAR) DNA‐binding protein of 43 kDa (TDP‐43) proteinopathy: a quantitative study using polynomial curve fitting

Armstrong

Hamilton

Hedreen

et al. 2013

Neuropathology Appl Neurobio

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“…Neuronal loss in upper cortex could be associated with degeneration of the feed-forward cortico-cortical projections, which have their cells of origin in laminae II/III [41]. By contrast, EN, which may reflect either a stress response or axonal degeneration [42,43], and glial cell nuclei, were frequently abundant in lower cortex. Pathological changes in lower cortex could be associated with degeneration of either the feedback cortico-cortical projections [41] or the afferent and efferent cortical-subcortical projections.…”

Section: Discussionmentioning

confidence: 98%

Cortical degeneration in frontotemporal lobar degeneration with TDP-43 proteinopathy caused byprogranulingene mutation

Armstrong

2014

International Journal of Neuroscience

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Familial frontotemporal lobar degeneration with transactive response (TAR) DNA-binding protein of 43 kDa (TDP-43) proteinopathy (FTLD-TDP) is most commonly caused by progranulin (GRN) gene mutation. To characterize cortical degeneration in these cases, changes in density of the pathology across the cortical laminae of the frontal and temporal lobe were studied in seven cases of FTLD-TDP with GRN mutation using quantitative analysis and polynomial curve fitting. In 50% of gyri studied, neuronal cytoplasmic inclusions (NCI) exhibited a peak of density in the upper cortical laminae. Most frequently, neuronal intranuclear inclusions (NII) and dystrophic neurites (DN) exhibited a density peak in lower and upper laminae, respectively, glial inclusions (GI) being distributed in low densities across all laminae. Abnormally enlarged neurons (EN) were distributed either in the lower laminae or were more uniformly distributed across the cortex. The distribution of all neurons present varied between cases and regions, but most commonly exhibited a bimodal distribution, density peaks occurring in upper and lower laminae. Vacuolation primarily affected the superficial laminae and density of glial cell nuclei increased with distance across the cortex from pia mater to white matter. The densities of the NCI, GI, NII, and DN were not spatially correlated. The laminar distribution of the pathology in GRN mutation cases was similar to previously reported sporadic cases of FTLD-TDP. Hence, pathological changes initiated by GRN mutation, and by other causes in sporadic cases, appear to follow a parallel course resulting in very similar patterns of cortical degeneration in FTLD-TDP.

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“…To examine the role of DRG SCs under pathological conditions, we challenged their response to nerve injury and questioned their participation in the regenerative process, using the same tracing paradigm as under physiological conditions ( Figure 5 A). Previous studies indicated that a variety of cellular changes occur in DRGs after sciatic nerve axotomy, including death of neurons and SGCs, followed by proliferation of microglia/macrophages, Schwann cells, and SGCs ( Cherkas et al., 2004 ; Hu and McLachlan, 2002 ; Pierucci and de Oliveira, 2006 ). We therefore performed unilateral sciatic nerve axotomy after tamoxifen induction of Nestin-CreER T2 /Rosa26-YFP (Nestin-YFP) mice.…”

Section: Resultsmentioning

confidence: 99%

Satellite glia of the adult dorsal root ganglia harbor stem cells that yield glia under physiological conditions and neurons in response to injury

Maniglier¹,

Vidal²,

Bachelin³

et al. 2022

Stem Cell Reports

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Increased sensory neuron apoptotic death 2 weeks after peripheral axotomy in C57BL/6J mice compared to A/J mice

Cited by 10 publications

References 32 publications

Laminar distribution of the pathological changes in sporadic frontotemporal lobar degeneration with transactive response (TAR) DNA‐binding protein of 43 kDa (TDP‐43) proteinopathy: a quantitative study using polynomial curve fitting

Laminar distribution of the pathological changes in sporadic frontotemporal lobar degeneration with transactive response (TAR) DNA‐binding protein of 43 kDa (TDP‐43) proteinopathy: a quantitative study using polynomial curve fitting

Cortical degeneration in frontotemporal lobar degeneration with TDP-43 proteinopathy caused byprogranulingene mutation

Satellite glia of the adult dorsal root ganglia harbor stem cells that yield glia under physiological conditions and neurons in response to injury

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