Role of oligodendrocytes and myelination in Alzheimer’s Disease: therapeutic perspectives targeting oligodendrocytes for the prevention and treatment of AD

March 16, 2020

Strasbourg (France)


This meeting takes place as a visioconference due to restrictions linked to coronavirus


Myelination is a developmental process which continues until the third decade of life in humans, following a precise temporal pattern with early and late myelinated regions. This prolonged period of myelination coincides with the occurrence of the massive remodeling of synaptic connections in the human cerebral cortex thought to underlie the experience-dependent modification of the brain. Interestingly, it has been suggested that, by differentiallly controlling the velocity of conduction in axons, myelin participates in synchronization mechanisms of impulse traffic.  This has led to the hypothesis that myelin might participate in information processing through experience, engendering some form of myelin plasticity complementary to synaptic plasticity. This previously unappreciated role of myelin in information processing and learning suggests that the disruptions in functional connectivity due to alterations in white matter structure might underlie impaired cognitive functions or disorganized thinking, for example. Indeed, if defects in myelin insulation can lead to impaired cognitive function in 40% of multiple sclerosis patients, they are also associated to a wide range of psychiatric disorders, such as schizophrenia and mood disorders. Interestingly, cognitive decline in aging and Alzheimer’s disease is also associated to changes in white matter, raising the possibility that myelin might play an unsuspected role in this disorder. Several clinical and basic studies have now well established that the brain white matter and myelin alterations are often among the earliest brain changes in Alzheimer's disease (AD), preceding the tangles and plaques. Moreover, white matter damage in aging and AD spreads in a relatively predictable pattern, with the latest structures to myelinate being the first to degenerate. These important findings have raised attention on the role of oligodendrocytes in myelin plasticity, and from there in dysfunction of information processing and AD. The potential role of oligodendrocyte failure and myelin loss suggest that innovating of strategies targeting oligodendrocytes might provide effective therapeutic options to prevent or treat AD.


This meeting takes place as a visioconference due to restrictions linked to coronavirus



10:00-10:15 Welcome address and Introduction (Mensah-Nyagan AG, Strasbourg, France)

10:15 – 11 :15 Superficial white matter in aging and Alzheimer's disease: what we know and what We should learn (Knyazeva M, Lausanne, Switzerland)

11:15 - 12:15 Myelin content changes in Mild Cognitive Impairment and Alzheimer’s disease, quantified by advanced brain MRI and associated with neuropsychiatric alterations (Papadaki E, Crete, Greece)

12:15 - 14:00 Lunch Break

14:00 - 15:00 Oligodendroglial Cells in Alzheimer's Disease (Butt A, Portsmouth, UK)

15:00 - 16:00 Single-cell transcriptomic analysis implicates oligodendrocytes and myelination in the pathophysiology of Alzheimer's disease (Mathys H, MIT-Cambridge, MA, USA)

16:00 - 16:15 Coffee Break

16:15 - 17:15 Senolytic therapy alleviates Aβ-associated oligodendrocyte progenitor cell senescence and cognitive deficits in an Alzheimer’s disease model
(Zhang P, NIH- Baltimore, MD, USA)

17:15 - 17:30 Closing Remarks


Monday, the 16th of March, 2020

This meeting takes place as a visioconference due to restrictions linked to coronavirus


Registration dead-line: March 9th, 2020

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This specific workshop will give rise to the attribution of 1 CP.

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