C1qB and clusterin mRNA increase in association with neurodegeneration in sporadic amyotrophic lateral sclerosis.
We analyzed postmortem tissues of sporadic amyotrophic lateral sclerosis (SALS) for mRNA levels of two inflammatory proteins, complement C1qB and clusterin (apoJ). By Northern blot hybridization, SALS was associated with increased mRNA for C1qB and clusterin in the motor cortex (Brodmann area A4), but not in superior temporal cortex (A17), relative to neurologically normal controls. By in situ hybridization, SALS spinal cords showed increased C1qB and clusterin mRNA in areas undergoing neurodegeneration. This evidence implicates inflammatory mechanisms during neurodegenerative processes in SALS.
Grewal
R P
RP
Department of Neurology, School of Medicine, University of Southern California, Los Angeles 90089-1340, USA. grewal@molbio.usc.edu
Morgan
T E
TE
Finch
C E
CE
D000293:Adolescent; D000368:Aged; D000369:Aged, 80 and over; D000690:Amyotrophic Lateral Sclerosis / Q000235:genetics* / Q000473:pathology; D002540:Cerebral Cortex / Q000378:metabolism* / Q000473:pathology; D051152:Clusterin; D015922:Complement C1q / Q000235:genetics*; D003169:Complement Inactivator Proteins / Q000235:genetics*; D005786:Gene Expression Regulation; D006023:Glycoproteins / Q000235:genetics*; D006801:Humans; D018832:Molecular Chaperones; D009410:Nerve Degeneration / Q000209:etiology / Q000235:genetics* / Q000473:pathology; D012333:RNA, Messenger / Q000235:genetics; D012016:Reference Values; D013003:Somatosensory Cortex / Q000378:metabolism; D013116:Spinal Cord / Q000378:metabolism* / Q000473:pathology; D013702:Temporal Lobe / Q000378:metabolism; D014158:Transcription, Genetic
C495242:CLU protein, human; D051152:Clusterin; D003169:Complement Inactivator Proteins; D006023:Glycoproteins; D018832:Molecular Chaperones; D012333:RNA, Messenger; D015922:Complement C1q