Culture models of neurodegenerative disease

Annals of the New York Academy of Sciences

Volumn 919, Issue , 2000, Pages 106-118

  Figlewicz, D A ^a   Dong, L ^a   Mlodzienski, M ^a   Turcotte, J C ^a  

^a UNIVERSITY OF ROCHESTER MEDICAL CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

MUTANT PROTEIN; SUPEROXIDE DISMUTASE;

ANIMAL CELL; APOPTOSIS; CELL COUNT; CELL CULTURE; CELL SIZE; CELL VIABILITY; CONFERENCE PAPER; DEGENERATIVE DISEASE; DISEASE MODEL; ENZYME ACTIVITY; IMMUNOCYTOCHEMISTRY; MOTONEURON; NONHUMAN; WESTERN BLOTTING;

ANIMALIA;

EID: 0033695001     PISSN: 00778923     EISSN: None     Source Type: Book Series    
DOI: 10.1111/j.1749-6632.2000.tb06873.x     Document Type: Conference Paper

References (11)

1. Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis
2. Purification of embryonic rat motor neurons by panning on a monoclonal antibody to the low affinity NGF receptor
3. Distinct regulatory pathways control neurofilament expression and neurotransmitter synthesis in immortalized serotonergic neurons
4. Glutamate potentiates the toxicity of mutant Cu/Zn superoxide dismutase in motor neurons by postsynaptic calcium-dependent mechanisms
5. Aggregation of mutant Cu/Zn superoxide dismutase proteins in a culture model of ALS
6. The univalent reduction of oxygen by reduced flavins and quinones
7. Early stages of motor neuron differentiation revealed by expression of homeobox gene Islet-1
8. Activation of protein kinase C induces neurofilament fragmentation, hyperphosphorylation of perikaryal neurofilaments, and proximal dendritic swellings in cultured motor neurons
9. Cell death: Current difficulties in discriminating apoptosis from necrosis in the context of pathological processes in vivo
10. Neuronal death in amyotrophic lateral sclerosis is apoptosis: Possible contribution of a programmed cell death mechanism
11. Lack of apoptosis in mice with ALS