Anti-Nogo-A antibody treatment does not prevent cell body shrinkage in the motor cortex in adult monkeys subjected to unilateral cervical cord lesion

BMC Neuroscience, 2008 · DOI: 10.1186/1471-2202-9-5 · Published: January 14, 2008

Simple Explanation

This study investigates whether treatment with anti-Nogo-A antibodies can prevent the shrinkage of nerve cell bodies in the motor cortex of monkeys after a spinal cord injury. The researchers compared monkeys treated with the antibody to those treated with a control substance after the injury. The results showed that while the antibody treatment helps nerve fibers sprout and recover in the spinal cord, it did not prevent the nerve cell bodies in the brain from shrinking. This suggests the antibody's effects are mainly focused on the nerve fibers near the injury site. The study concludes that anti-Nogo-A antibody treatment primarily affects the distal parts of the injured nerve cells, particularly promoting axon collateralization in the cervical cord, but has little impact on the cell bodies themselves.

Study Duration

Not specified

Participants

Intact monkeys (n = 5); monkeys with cervical lesion and treated with control antibody (n = 4); monkeys with cervical lesion and treated with anti-Nogo-A antibody (n = 5).

Evidence Level

Level II: Experimental study in primates

Key Findings

1
Unilateral cervical lesion does not lead to significant neuronal loss of corticospinal (CS) neurons in the contralesional hemisphere.
2
Anti-Nogo-A antibody treatment enhances axonal sprouting in the cervical cord, but does not prevent soma shrinkage of axotomized CS neurons.
3
Soma shrinkage of CS neurons occurs in the contralesional hemisphere in both control antibody and anti-Nogo-A antibody treated monkeys after cervical lesion.

Research Summary

The study investigates the effect of anti-Nogo-A antibody treatment on cell body shrinkage in the motor cortex of monkeys after unilateral cervical cord lesion. The findings indicate that anti-Nogo-A treatment does not prevent soma shrinkage of axotomized CS neurons, suggesting that the antibody primarily affects distal axon collateralization. The results confirm that cervical cord lesion does not cause significant loss of CS neurons, which is a favorable outcome for potential functional recovery through axonal sprouting.

Practical Implications

Targeted Therapies

Future therapies should consider directly addressing soma shrinkage in addition to promoting axonal sprouting.

Localized Action of Antibodies

The anti-Nogo-A antibody's effect is primarily at the lesion site, indicating the need for strategies to enhance its impact on cell bodies in the motor cortex.

Combination Therapies

Combining anti-Nogo-A treatment with interventions targeting neuronal metabolism and trophic support may yield better outcomes.

Study Limitations

1
The study focused on soma size and may not capture other morphological changes in CS neurons.
2
The dose and delivery method of the anti-Nogo-A antibody may have limited its effect on cortical cell bodies.
3
The hindlimb area of M1 was analyzed, and the findings may not fully represent effects in the hand area.

Your Feedback

Was this summary helpful?

Back to Spinal Cord Injury