Biomedical subjects

Thomas Möller

Publications and source records attributed to Thomas Möller.

21 records · Page 2Linked to original sources

PubMed2003

Assessing disease onset and progression in the SOD1 mouse model of ALS.

SOD1 transgenic mice are the most widely used animal model of amyotrophic lateral sclerosis (ALS). In addition to providing valuable insights into the pathogenesis of ALS, these animals are used intensively in many laboratories as an in vivo model for investigating novel therapeutic interventions towards this devastating motorneuron disease. Such pre-clinical studies require objective and reliable quantification of the clinical phenotype of individual mice, most importantly of the neuromuscular abnormalities. Here we compare four parameters of the clinical phenotype: motor signs, body weight, rotarod performance and paw grip endurance for their usefulness in monitoring the SOD1 mouse model. We found that paw grip endurance is a sensitive and inexpensive alternative to the widely used rotarod test.

Age of Onset↗

PubMed2002

Calcium signaling in microglial cells.

Receptor-mediated Ca(2+) signals are a common signal transduction mechanism in all living cells, including microglia. Recent years have brought major advances in our understanding of microglial Ca(2+) signaling. More than 20 receptor/ligand interactions leading to Ca(2+) signals in microglia have been described so far, and it seems that this is just the beginning. The literature has grown rapidly during the past few years, especially in regard to chemokine and ATP/UTP receptor signaling. This article presents a brief overview of the basics of Ca(2+) signaling, reviews the current literature on microglial Ca(2+) signaling, and discusses the current challenges and possible future directions of this emerging field.

Animals↗

PubMed2002

Neuro-inflammation as a therapeutic target in amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis (ALS) is a rapidly progressive neuromuscular disease that destroys both upper and lower motor neurons, resulting in spasticity, diffuse muscular atrophy, weakness, and ultimately death from respiratory failure. It is presumed that in the vast majority of cases, ALS is acquired and occurs sporadically, although the exact etiology is unknown. Recent, emerging evidence suggests that neuro-inflammation may be a pathological characteristic of this disease; this could represent a potential therapeutic target for a pharmacological agent to help treat this severe disease. This article reviews the current research in this area and discusses theoretical and clinical ramifications of these recent findings.

Amyotrophic Lateral Sclerosis↗