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Scientists at Baylor College of Medicine, Texas Children's Hospital and partner institutions said they have found that genetic variants associated with Alzheimer’s risk can disrupt The protective mechanism of the brain, which leads to neurodegeneration
In this study, “the formation of glial lipid droplets induced by neuron ros was altered by the loss of Alzheimer’s disease-related genes,” an article published in the Proceedings of the National Academy of Sciences (PNAS) also revealed The evidence supports reactive oxygen species (ROS), which is a natural by-product of cell metabolism, is related to inflammation and other processes, and is a key factor leading to the destruction of neuroprotective mechanisms
In short, these findings seem to provide a new mechanism for the development of Alzheimer's disease and support the idea that multiple changes at the genetic and other cellular levels combine to induce disease
More and more genetic risk factors for Alzheimer's disease (AD) are being identified, but the contribution of each variant to the disease mechanism is still largely unknown
"In order to determine the proteins that regulate these neuroprotective effects, we tested the role of AD risk genes in the formation of ros-induced LD, and proved that several genes affect the formation of neuroprotective LD, including human ABCA1, ABCA7, VLDLR, VPS26, Homologs of VPS35, AP2A, PICALM and CD2AP
"Finally, the peptide agonist of ABCA1 can restore the formation of glial LD in the humanized APOE4 Drosophila model, which provides a potential therapeutic approach to prevent ros-induced neurotoxicity
"Previous work by Dr.
When neurons are faced with high levels of ROS, neuroprotective mechanisms come into play, stimulating neurons to produce rich lipids
In previous studies, the researchers linked the neuroprotective mechanism to the strongest genetic risk factor for Alzheimer's disease, the apolipoprotein APOE4
Moulton pointed out: "In our current work, we want to identify genes that are essential for lipid droplet formation, especially those that are required for the export of lipids from neurons and the introduction of lipids into glial
Morton added: "In all cases where ROS was present, we saw droplet loss and we also saw neurodegeneration, again proving that the interference of glial cell droplet formation can cause neuron damage
In this way, the team demonstrated that several genes related to the risk of Alzheimer’s disease in the whole-genome sequencing study disrupted the formation of neuroprotective lipid droplets, which provided a mechanism that could explain the risks associated with these genes.
In addition, in the Drosophila model, Moulton and his colleagues tested whether the ABCA1 agonist can enable APOE4 in the Drosophila model to mediate the formation of lipid droplets in glial cells
The researchers also studied whether ROS can exacerbate the effects of amyloid on the disease
Moulton pointed out: "We observed that ROS and amyloid-β together increase the death of Drosophila neurons and lead to larger and more amyloid-rich plaques in the mouse model, which shows that indeed ROS and amyloid-β can interact and may affect the progression of the disease
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"As we age, the ROS in the brain will increase
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If another mutation disrupts the path of the droplets, then neurons will become sensitive to the accumulation of lipid droplets, paving the way for neurodegeneration
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"Our research results support further research on feasible ways to reduce the level of ROS in the brain as a strategy to reduce the key effect of ROS on neurodegeneration
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"
