In Vivo PET Imaging of Myelin Damage and Repair in the Spinal Cord
Abstract
One of the major challenges to developing new treatments for demyelinating diseases such as Multiple Sclerosis (MS) is generating unambiguous data that the treatment is working, and more importantly that it is working through identifiable mechanisms. The majority of the current treatments available to patients with MS are targeted toward suppressing the immune system and its attack on myelin, oligodendrocytes and axons of the brain and spinal cord. Loss of myelin results in the failure of efficient conduction of axonal impulses leading to various neurological disabilities and cognitive impairment. In the healthy CNS, demyelinated axons can be reinvested with new myelin sheaths through an effective regenerative process. The remyelination process is thought to involve the recruitment of oligodendrocyte precursor cells (OPCs) that are subsequently activated and distributed to the damaged axons. However, the remyelination process is often disrupted in MS. This leads to incomplete myelin repair, and subsequent irreversible axonal damage. Given the central role the loss of myelin is thought to play in the generation of functional deficits in MS, my laboratory has spent the last 15 years trying to identify new ways to promote myelin repair. The overarching concept is that perhaps the combination of the inhibition of immune attack and the promotion of myelin repair within the CNS will generate more effective therapeutic approaches. This notion leads to the question of how to identify myelin repair in a longitudinal study of MS patients. Currently, the only way to unambiguously show myelin repair is through histological analyses of autopsy or biopsy material.
Document Details
- Document Type
- Technical Report
- Publication Date
- Oct 01, 2012
- Accession Number
- ADA575626
Entities
People
- Robert H. Miller
Organizations
- Case Western Reserve University