Who Knew What Tau In Oligodendrocytes Can Do?

Being tuned in to the changes in life and staying current makes you young at heart. As life evolves, the ability to adapt moves your life forward, allowing you to thrive. By contrast, functional rigidity would undermine health and, ultimately, life itself. The brain, our most magical place, allows us to imagine, remember, and move.

In the brain, cells called oligodendrocytes (OLGs) surround the axons with myelin as these cells can extend cellular processes. It is ultimately the correct thickness of the myelin around the axon that makes it possible for humanity to function.


Recent studies have shown that what makes cellular process extension and myelination possible is not a one-time life event occurring largely at postnatal life. Such events persist indeed for an entire lifetime during the many challenges of life. For OLGs to extend cellular processes and form myelin, the cytoskeleton protein tau must properly function in these cells. The function of tau relies on its ability to bind to the cytoskeleton and regulate various cell functions. By contrast, when tau cannot bind the cytoskeleton, cells cannot transport critical loads within the cells, cells cannot recycle proteins, and cell functions break down not only for OLGs but also for neurons.

The neurons are indeed lifelong partners of OLGs, depending on healthy myelin to properly function. Tau consists of various tau protein isoforms due to precise regulation. Complexity is derived also from highly-regulated phosphorylation and other post-translational modifications. Finely-tuned tau protein function is required early in life and during a lifetime. Should tau in OLGs fail the support of cellular processes, neuronal demise would follow.

Both animal studies and clinical evidence have shown that a defect of tau in OLGs causes defects in myelin and neuronal functions, often resulting in abnormal gait. Furthermore, the ability of neuronal activity to modulate myelin sets it as an essential player, making possible both brain health and plasticity. It is well established that the abnormal phosphorylation of tau is present and characterizes diseases of memory. Such diseases include Alzheimer’s disease and other diseases with alterations in cognitive functions, some of which have a pathology of tau in OLGs.


Usually, myelin must be healthy for proper brain function. In Alzheimer’s disease, myelin alteration has been recognized as a quite early event, and such early anomaly seems to prime progressive central nervous system degeneration. The regulation of tau as OLGs embark in the challenge of a lifetime is largely unknown. In particular, experience-based regulation of tau in OLGs must be considered a potential new therapeutic approach to prevent and treat dysfunctions in cognitive functions. Thus, Alzheimer’s research focused on tau in OLGs might provide new therapeutic avenues to prevent and treat this devastating disease and other forms of dementia.

Due to the lack of effective therapeutic approaches for this disease, the research on tau in OLGs might reveal new avenues for the understanding and treatment of many forms of dementia.

These findings are described in the article entitled Tau in Oligodendrocytes Takes Neurons in Sickness and in Health, recently published in the International Journal of Molecular Sciences.

About The Author

Patrizia LoPresti has received training at major universities, including Penn and the University of Chicago. She has made significant contributions in advancing the field of the cytoskeleton in oligodendrocytes and multiple sclerosis, and more recently her work has contributed to understand cognitive decline as an early event during multiple sclerosis disease.