0000000000920645
AUTHOR
Lucía Galán
Clinical and therapeutic features of myasthenia gravis in adults based on age at onset
[Objective] To describe the characteristics of patients with very-late-onset myasthenia gravis (MG).
Amyotrophic lateral sclerosis modifies progenitor neural proliferation in adult classic neurogenic brain niches.
Background Adult neurogenesis persists through life at least in classic neurogenic niches. Neurogenesis has been previously described as reduced in neurodegenerative diseases. There is not much knowledge about is adult neurogenesis is or not modified in amyotrophy lateral sclerosis (ALS). All previous publications has studied the ALS SOD1 (superoxide dismutase) transgenic mouse model. The purpose of this study is to examine the process of adult neurogenesis in classic niches (subventricular zone [SVZ] and subgranular zone [SGZ] of the dentate gyrus) in patients with amyotrophic lateral sclerosis (ALS), both with (ALS-FTD) and without associated frontotemporal dementia (FTD). Methods We stud…
Additional file 1: Table S1. of Amyotrophic lateral sclerosis modifies progenitor neural proliferation in adult classic neurogenic brain niches
Antibodies used in the immunohistochemical study. Table S2. Summary of patient characteristics. Table S3. Immunohistochemical studies used in ALS diagnosis. Values for TDP-43 and ubiquitin are expressed in inclusions per field; %pTDP-43 represents the percentage of phosphorylated TDP inclusions out of the total. Table S4. Description of neurogenesis patient to patient. Table S5. Neurogenesis findings in the subgranular zone of the hippocampal dentate gyrus, by patient. Table S6. Summary of results in the SVZ. Table S7. Summary of results in the hippocampus. (DOC 302 kb)
Subventricular zone in motor neuron disease with frontotemporal dementia.
Investigate how the subventricular proliferation and organisation is modified in a patient with FTLD-ALS. We studied the subventricular zone (SVZ) of a patient with FTLD-ALS immunohistochemical and histologically. We found an increase of Ki-67 positive cells and neuroblast in the subventricular zone, suggesting an activation of proliferating activity in response to FTD-ALS. This proliferation can act as a compensatory mechanism for rapid neuronal death and its modulation could provide a new therapeutic pathway in ALS. These results suggest a modification of neurogenesis in FTD-ALS. (C) 2011 Elsevier Ireland Ltd. All rights reserved.