Abstract:
:In the superoxide dismutase 1 (SOD1)(G93A G1H) transgenic mouse, the primary pathology and disease signs are associated with the degeneration of motor neurons in the lumbar spinal cord. It is unclear if the descending motor pathways from the cortex and brainstem are also compromised. The retrograde tracer Fluorogold was inserted into the T(12) segment of the spinal cord and the number of labelled neurons counted in the sensorimotor cortex and brainstem of 60, 90 and 110 day-old mice. A small loss of corticospinal and bulbospinal projections was detected at 60 days. By 110 days, 53% of corticospinal, 41% of bulbospinal and 43% of rubrospinal neurons were lost. The progressive loss of corticospinal axons was confirmed using the stereological fractionator method. These findings suggest that the expression of the SOD1(G93A G1H) mutant protein results in a disease that resembles the late stages of human motor neuron disease. This involves not only the destruction of lower motor neurons in the spinal cord, but also additional loss of descending cortical and bulbar neurons.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Zang DW,Cheema SSdoi
10.1016/s0304-3940(02)00944-8keywords:
subject
Has Abstractpub_date
2002-10-31 00:00:00pages
99-102issue
2eissn
0304-3940issn
1872-7972pii
S0304394002009448journal_volume
332pub_type
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