Multiple Sclerosis & Neuroinflammation Treatment

Multiple sclerosis is understood clinically through its relapses—acute episodes of demyelination that produce visible lesions on MRI and measurable neurological deficits. Disease-modifying therapies target the adaptive immune mechanisms that produce those relapses, and they do so with increasing effectiveness. But relapse biology is not the whole disease.

Trapp and Nave documented in 2008 that progressive axonal loss occurs in MS independently of acute inflammatory lesions. Axons degenerate in normal-appearing white matter, in cortical gray matter, and in regions that never showed gadolinium enhancement on MRI. This slow, cumulative axonal injury is what drives the disability accumulation that patients experience between relapses and that accelerates in progressive disease.

Lassmann expanded this understanding in 2018, demonstrating that neurodegeneration in MS is not simply collateral damage from relapsing inflammation. It is a partially independent process sustained by chronic microglial activation, oxidative injury to mitochondria, and energy failure in demyelinated axons. The innate immune system—microglia and astrocytes—remains activated even when the adaptive immune response has been suppressed by therapy. This is why patients on effective DMTs can still accumulate disability over time.

At the cellular level, Mahad et al. (2015) showed that mitochondrial dysfunction is a central driver of neurodegeneration in MS. Demyelinated axons require dramatically more energy to conduct signals, because they must redistribute ion channels along their entire length rather than relying on saltatory conduction at nodes of Ranvier. When mitochondria in those axons cannot meet the increased energy demand—due to oxidative damage to respiratory chain complexes, NAD+ depletion, and impaired mitophagy—the axon degenerates. The neuron dies not from an immune attack, but from an energy crisis.

We want to be direct about this, because it matters. The Neurogenesis Project does not replace disease-modifying therapy for MS. We do not prescribe DMTs, we do not adjust DMTs, and we do not advise patients to stop or change their DMT regimen. That responsibility belongs to the neurologist managing your MS, and it stays there.

What we offer is a complementary layer of care that most MS patients cannot access through their standard treatment team. Disease-modifying therapy addresses the immune-mediated component of the disease. Our protocols address the metabolic and regenerative component—mitochondrial support, oxidative stress reduction, cellular signaling for repair, and advanced monitoring of subclinical disease activity. These two approaches are not in competition. They target different aspects of the same disease.

Every patient who comes to us with an MS diagnosis is evaluated in the context of their existing care. We review their DMT history, MRI trajectory, relapse frequency, and current treatment plan before designing any protocol. We communicate with their neurologist. And we structure our therapies to complement—never contradict—the immunological strategy already in place.

Standard MS monitoring focuses on relapse frequency and new lesion formation on MRI. These are essential metrics, but they do not capture the subclinical neurodegeneration, mitochondrial dysfunction, and oxidative stress that continue between relapses. Our diagnostic evaluation measures what standard MS care does not.

Advanced MRI Protocols. Beyond conventional T2 and FLAIR sequences, we evaluate brain volume metrics, cortical lesion burden, and normal-appearing white matter changes. Volumetric analysis tracks brain atrophy rates over time—a more sensitive marker of progressive neurodegeneration than lesion counts alone.

Neurofilament Light Chain (NfL). Serum neurofilament light chain is a biomarker of ongoing axonal injury. Elevated NfL levels indicate active neurodegeneration even in the absence of clinical relapses or new MRI lesions. We use serial NfL measurements to monitor subclinical disease activity and to assess treatment response over time.

Optical Coherence Tomography (OCT). OCT measures retinal nerve fiber layer thickness and ganglion cell layer volume—direct measures of axonal and neuronal integrity in the central nervous system. Retinal thinning in MS correlates with brain atrophy and disability progression, providing a non-invasive window into neurodegenerative activity that MRI cannot capture at the same resolution.

Inflammatory & Metabolic Panels. We measure inflammatory cytokines (IL-6, TNF-alpha, IL-17), oxidative stress markers (F2-isoprostanes, 8-OHdG), mitochondrial function indices, and comprehensive metabolic panels. These labs distinguish patients with active subclinical inflammation from those whose progression is driven primarily by mitochondrial failure or oxidative damage—a distinction that shapes the treatment protocol.