In a recent study published in the journal PLOS Biology , researchers used mouse models to demonstrate that neurons were not the only source of abnormal amyloid β proteins contributing to the pathology of Alzheimer's disease. They found that oligodendrocytes play a significant role in the abnormal neuronal hyperactivity in Alzheimer's disease and are a major source of amyloid β protein. Study: Selective suppression of oligodendrocyte-derived amyloid beta rescues neuronal dysfunction in Alzheimer’s disease .
Image Credit: nobeastsofierce / Shutterstock Background The accumulation of abnormal amyloid β plaques is one of the hallmarks of Alzheimer's disease. Amyloid β plaques are an important target for therapy and understanding the disease's pathophysiology. Clinical trials for antibodies against amyloid β have shown that targeting amyloid β plaques slows the functional and cognitive decline in Alzheimer's patients.
One of the first neuronal responses to the accumulation of amyloid β plaques is increased and abnormal excitability. Transcriptomics-based research has shown that astrocytes, microglia, and oligodendrocytes in mouse models of Alzheimer's disease and Alzheimer's disease tissue from humans show abnormal responses to amyloid β. However, despite these observed cellular effects of amyloid β, the possibility of other cells in the nervous system being sources of aberrant amyloid β has not been explored.
About the study In the present study, the researchers expl.