A study in Nature Neuroscience found that both neurons and oligodendrocytes contribute to amyloid-β plaque burden in Alzheimer's disease, highlighting new therapeutic targets.
By Dr. Sushama R. Chaphalkar, PhD.Reviewed by Susha Cheriyedath, M.Sc.Aug 7 2024 In a recent study published in the journal Nature Neuroscience , researchers investigated the contributions of oligodendrocytes and neurons to amyloid-β plaque burden in Alzheimer's disease 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.
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 . However, recent studies suggest that other cell types may also produce Aβ.
Results and discussion According to the study, both neurons and OLs were found to express amyloidogenic pathway genes. APP expression in OLs was confirmed in both murine and human tissues. Novel AD mouse lines revealed a 30% reduction in plaque burden in OL-Bace1cKO;AD mice compared to controls, while ExN-Bace1cKO;AD mice showed a 95–98% reduction. This indicated that ExN-derived Aβ is crucial for plaque formation.
Working model of modulating cell-type-specific Aβ contributions. Selectively ablating Aβ from specific cell types results in steady-state rate change of Aβ production, causing exponentially slower plaque growth that follows a sigmoidal growth curve. ctrl, control; rel., relative.
Alzheimer's Disease Cell Dementia Genes In Vivo Myelin Neurodegenerative Disorder Neurons Neuroscience Pathology
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