Cece wrote:I don't think it'll help us much in MS because in MS, axons are not severed, so there's nothing to relink.
Cece wrote:You are suggesting that axons are severed in MS? This advancement is specifically a way to get a severed axon to reattach to the neuron body.
From Oxford Brain Journal wrote:In recent years, it has become more evident that axonal damage is the major morphological substrate of permanent clinical disability. In our study, we investigated the occurrence of acute axonal damage determined by immunocytochemistry for amyloid precursor protein (APP) which is produced in neurones and accumulates at sites of recent axon transection or damage.
Transected axons were a consistent feature of the lesions of multiple sclerosis, and their frequency was related to the degree of inflammation within the lesion. The number of transected axons per cubic millimeter of tissue averaged 11,236 in active lesions, 3138 at the hypocellular edges of chronic active lesions, 875 in the hypocellular centers of chronic active lesions, and less than 1 in normal-appearing white matter from the control brains.
Axonal transection occurs at sites of inflammation and begins at disease onset but is clinically silent in RR-MS because the CNS compensates for neuronal loss. Once a threshold of axon loss is ex ceeded, MS patients enter an irreversible secondary progressive stage. In SP-MS, axonal degeneration is caused by chronic demyelination and may be irreversibly progressive. This view of MS provides a concep tional framework that explains conversion of RR-MS to SP-MS and provides a rationale for early aggressive anti-inflammatory and neuroprotective therapies.
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