S12  Emerging views on microglia and oligodendrocytes in Alzheimer's disease

Klaus-Armin Nave (Göttingen)

Live Discussion: Wednesday, March 24, 2021, 18:00 - 19:00h

Brain aging is considered the main risk factor of Alzheimer’s disease. However, the cellular mechanisms that link aging to the pathological hallmarks of AD are largely unclear. Morphological changes that can be detected in healthy brains at an advanced age could point to these age-dependent AD risk factors. Ultrastructural features of mammalian brain aging include oligodendrocyte and myelin abnormalities associated with low-grade inflammation. Myelin-forming oligodendrocytes are of specific interest because they provide metabolic support to axons and loss of myelin triggers secondary inflammation. Microglial cells themselves are subject to age-dependent changes that affect their ability to clear amyloid deposits and lead to a proinflammator phenotype. This symposium highlights novel disease models and preclinical findings that demonstrate a previously overlooked role of oligodendrocytes and microglia in driving the neuropathologic changes of AD.

S12-1 Madeline Nicholson, Parkville, Australia
Oligodendrogenesis declines during healthy aging in the mouse central nervous system and is mediated by neuronal BDNF-TrkB signalling

S12-2 Xin Qi, Cleveland, USA
Oligodendrocyte dysregulation in Alzheimer’s disease

S12-3 Constanze Depp, Goettingen, Germany
Aging-associated oligodendrocyte dysfunction drives amyloid deposition in Alzheimer’s disease

S12-4 Michael Thomas Heneka, Bonn, Germany
Innate immune activation in neurodegenerative disease

S12-5 Carla Cangalaya, Magdeburg, Germany
Synaptic remodeling in response to acute microglia activation using light-induced engagement of microglia in the adult brain

S12-6 Christian Haass, Munich, Germany
Therapeutic Modulation of TREM2 Function