In a recent study published in the journal Nature Neuroscience , researchers investigated the contributions of oligodendrocytes (OLs) and neurons to amyloid-β (Aβ) plaque burden in Alzheimer's disease (AD) model mice. They found that OLs and neurons add to Aβ plaque burden, wherein excitatory projection neurons need to provide a threshold level of Aβ for rapid plaque seeding. The findings are valuable for understanding AD prevention and potentially inform therapeutic strategies.
Study: Oligodendrocytes produce amyloid-β and contribute to plaque formation alongside neurons in Alzheimer’s disease model mice . Image Credit: Jose Luis Calvo / Shutterstock Background AD is a progressive neurodegenerative disorder characterized by memory loss, cognitive decline, and behavioral changes. It commonly leads to dementia among older adults.
It involves the accumulation of Aβ plaques and neurofibrillary tangles in the brain, leading to the death of brain cells and the deterioration of brain function. Evidence suggests that Aβ production is mainly linked to excitatory neurons (ExNs). However, recent studies suggest that other cell types may also produce Aβ.
Studies have shown that cultured OLs can generate detectable levels of Aβ in vitro . Given that OL lineage cells are abundant in both gray and white matter, and myelin changes are known to be associated with AD, researchers in the present study investigated whether OLs contribute to Aβ plaque burden in vivo . They aimed to u.