The multiple levels of protection against neurodegeneration offered by DC-TAB are all relevant to ALS. The ability of DC-TAB to suppress the formation of toxic aggregates of for example superoxide dismutase 1, but also of other protein aggregates in the CNS, has been well documented. Very small quantities of DC-TAB are already adequate to stop such aggregates from forming, or even to dissolve existing aggregates. This eliminates their neurotoxic effects. In addition, DC-TAB counteracts oxidative stress, a likely key factor that promotes the formation of such toxic protein aggregates in the first place. DC-TAB also induces powerful neuroprotective responses by microglia that lead to additional secondary protective responses by neighboring astrocytes in the CNS. These collectively increase neuronal survival, suppress inflammatory damage and help prevent neuronal death by excitotoxicity. Finally, DC-TAB will promote the development of neuroprotective regulatory T cells in the periphery.

Simultaneous and complementary intervention at these different levels rather than inhibition of one specific disease pathway renders DC-TAB uniquely suited to inhibit the disease process in ALS, which is likely driven by multiple pathogenic factors rather than one. Emphasizing the therapeutic potential of DC-TAB, a selective link has recently been demonstrated between high levels of alpha B-crystallin in the spinal cord of mice with experimentally induced ALS, and markedly delayed onset of disease symptoms and improved survival of these animals.

DC-TAB intervenes at multiple levels in the disease process that drives ALS. It eliminates neurotoxic protein aggregates and promotes development of neuroprotective regulatory T cells. By activating microglia, DC-TAB induces production of a protective cocktail of soluble factors that support neuronal survival and suppress inflammation and oxidative stress. Some of these factors go on to activate a secondary, complementary protective response by neighboring astrocytes. This multi-level intervention renders DC-TAB uniquely suited to target ALS, which is likely caused by the combined impact of multiple pathogenic factors.