Multiple sclerosis

Multiple sclerosis often strikes between the ages of 20 and 40, when people are entering the workforce and raising families.

Emerging evidence points to a viral infection, low levels of vitamin D and genetics as culprits in multiple sclerosis, but how they combine to cause the disease is unclear.

New drugs are beginning to show promise for people with one of the less common, and harder to treat, forms of multiple sclerosis.

It is time for a bolder approach to developing drugs for progressive multiple sclerosis, says Bibi Bielekova.

Could a high-risk treatment play a part in tackling multiple sclerosis?

Dietary changes may be able to alleviate the symptoms of multiple sclerosis, but testing the effects of diet will need a different protocol to the one used for drugs.

In this Review, Mishra and Yong consider how myeloid cells — monocytes, macrophages, microglia and dendritic cells — contribute to the pathology of multiple sclerosis (MS). The authors also consider how current multiple sclerosis treatments might directly and indirectly affect these cells.

Stress can induce expression of norepinephrine, which can enhance neuroinflammation. Shaked, Hedrick and colleagues show that the transcriptional repressor Nr4a1 limits this stress-induced response by suppressing expression of tyrosine hydroxylase required for the synthesis of norepinephrine.

Ischaemia damages nerve myelin by depriving neurons and their myelinating oligodendrocytes of oxygen and glucose; here it is shown that ischaemic damage is caused through the H⁺-dependent activation of TRPA1 channels, and not via glutamate receptors of the NMDA type, as previously thought, providing a new mechanism and promising therapeutic targets for diseases as diverse and prevalent as cerebral palsy, spinal cord injury, stroke and multiple sclerosis.

MRI-based visualization of demyelinated CNS lesions is pivotal to the diagnosis and monitoring of multiple sclerosis (MS). The authors describe how advanced multimodal neuroimaging techniques are providing valuable insights into lesion structure and blood–brain barrier dynamics, thereby narrowing the gap between the macroscopic view of the radiologist and the microscopic view of the pathologist. The findings in humans are compared with data from a primate model of MS — experimental autoimmune encephalomyelitis in the common marmoset.

Research on the blood–brain barrier (BBB) has led to the concept of a complex, dynamic interface between the central nervous system (CNS) and periphery. Banks considers how this new understanding can combine with classical concepts to inform CNS drug delivery strategies and promote BBB integrity in various diseases.