LCM-based microarray analysis of TAU-P301L and SOD1-G93A motor neurons and surrounding glial cells

ABSTRACT: Familial amyotrophic lateral sclerosis (ALS) represents about 10% of ALS cases. In about 20% of familial ALS patients, a mutation in superoxide dismutase-1 (SOD1) can be found. The ubiquitous SOD1 protein converts superoxide radical anions to oxygen and hydrogen peroxide. Patients with familial ALS caused by mutations in SOD1 can show comorbidity with frontotemporal dementia and develop cognitive impairment, including apathy, inattention, verbal deficits, and hypersexuality. At the cellular level, pathological signs of ALS may include tau immunoreactive astrocytic and neuronal inclusions, suggesting that cognitive dysfunction in ALS may also reflect abnormal protein metabolism of the microtubule associated protein (MAP), tau. To identify cell-specific expression changes, we performed laser

ORGANISM(S): Mus musculus

SUBMITTER: Stanislav Karsten 

PROVIDER: E-GEOD-22482 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress