Deficiency of complement defense protein CD59 may contribute to neurodegeneration in Alzheimer's disease

Journal of Neuroscience

Volumn 20, Issue 20, 2000, Pages 7505-7509

  Yang, L B ^a   Li, R ^a   Meri, S ^a   Rogers, J ^a   Shen, Y ^a  

^a SUN HEALTH RESEARCH INSTITUTE   (United States)

Author keywords

Alzheimer; Amyloid protein; Complement; Inflammation; Neurodegeneration; Neuron death

Indexed keywords

AMYLOID BETA PROTEIN; CD59 ANTIGEN; COMPLEMENT COMPONENT C9; COMPLEMENT MEMBRANE ATTACK COMPLEX; LACTATE DEHYDROGENASE; MESSENGER RNA; PHOSPHOLIPASE C;

AGED; ALZHEIMER DISEASE; ARTICLE; CLINICAL ARTICLE; CONTROLLED STUDY; ENZYME LINKED IMMUNOSORBENT ASSAY; FEMALE; FRONTAL CORTEX; HIPPOCAMPUS; HUMAN; HUMAN CELL; HUMAN TISSUE; MALE; NERVE DEGENERATION; PRIORITY JOURNAL;

EID: 0034667686     PISSN: 02706474     EISSN: None     Source Type: Journal    
DOI: 10.1523/jneurosci.20-20-07505.2000     Document Type: Article

References (25)

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9. Determination of the active site of CD59 with synthetic peptides
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16. GPI anchored cell-surface molecules complexed to protein tyrosine kinases
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20. Human neurons derived from a teratocarcinoma cell line express solely the 695-amino acid amyloid precursor protein and produce intracellular-amyloid or A4 peptides
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