Recommended Conferences

Human Genetics and Genetic Disorders

Miami, USA

Tissue Engineering and Regenerative Medicine

Chicago, USA
Related Subjects

Complement component C1q inhibits beta-amyloid- and serum amyloid P-induced neurotoxicity via caspase- and calpain-independent mechanisms

Author(s): Pisalyaput K, Tenner AJ


Alzheimer’s disease is a neurodegenerative disorder characterized by neuronal loss, β-amyloid (Aβ) plaques, and neurofibrillary tangles. Complement protein C1q has been found associated with fibrillar Aβ deposits, however the exact contributions of C1q to Alzheimer’s disease is still unknown. There is evidence that C1q, as an initiator of the inflammatory complement cascade, may accelerate disease progression. However, neuronal C1q synthesis is induced after injury/infection suggesting that it may be a beneficial response to injury. In this study, we report that C1q enhances the viability of neurons in culture and protects neurons against Aβ- and serum amyloid P (SAP)-induced neurotoxicity. Investigation of potential signaling pathways indicates that caspase and calpain are activated by Aβ, but C1q had no effect on either of these pathways. Interestingly, SAP did not induce caspase and calpain activation, suggesting that C1q neuroprotection is in distinct from caspase and calpain pathways. In contrast to Aβ- and SAP-induced neurotoxicity, neurotoxicity induced by etoposide or FCCP was unaffected by the addition of C1q, indicating pathway selectivity for C1q neuroprotection. These data support a neuroprotective role for C1q which should be further investigated to uncover mechanisms which may be therapeutically targeted to slow neurodegeneration via direct inhibition of neuronal loss.

Similar Articles

Rat hippocampal neurons in dispersed cell culture

Author(s): Banker GA, Cowan WM

C1q induction and global complement pathway activation do not contribute to ALS toxicity in mutant SOD1 mice

Author(s): Lobsiger CS, Boillee S, Pozniak C, Khan AM, McAlonis-Downes M, et al.

A dramatic increase of C1q protein in the CNS during normal aging

Author(s): Stephan AH, Madison DV, Mateos JM, Fraser DA, Lovelett EA, et al.

When, where, and how much? Expression of the Kv3

Author(s): Gan L, Kaczmarek LK


Author(s): Yasuda T, Cuny H, Adams DJ

A-type K+ channels encoded by Kv4

Author(s): Carrasquillo Y, Burkhalter A, Nerbonne JM

Functional specialization of the axon initial segment by isoform-specific sodium channel targeting

Author(s): Boiko T, van Wart A, Caldwell JH, Levinson SR, Trimmer JS, et al.

Role of axonal NaV1

Author(s): Royeck M, Horstmann MT, Remy S, Reitze M, Yaari Y, et al.

The role of the Rho GTPases in neuronal development

Author(s): GovekEE, Newey SE, van Aelst L

EphB-mediated degradation of the RhoA GEF Ephexin5 relieves a developmental brake on excitatory synapse formation

Author(s): Margolis SS, Salogiannis J, Lipton DM, Mandel-Brehm C, Wills ZP, et al.

Potential role of culture mediums for successful isolation and neuronal differentiation of amniotic fluid stem cells

Author(s): Orciani M, Emanuelli M, Martino C, Pugnaloni A, Tranquilli AL, et al.