Researchers have made a groundbreaking discovery about the death of neurons in Alzheimer’s disease. A recent study reveals that neurons undergo programmed cell death, called necroptosis, when exposed to amyloid plaques and tau tangles, which are hallmark proteins associated with the disease. The study identifies an RNA gene called MEG3 as a potential key player in this process. This significant finding opens up promising pathways for future treatments of Alzheimer’s.
Previous research has shown that neurons exposed to amyloid plaques and tau tangles initiate necroptosis, a form of programmed cell death. In this current study, researchers observed that human neurons specifically displayed Alzheimer’s characteristics when exposed to these proteins, suggesting human-specific factors contributing to the disease. This finding challenges previous mouse models of Alzheimer’s, which could not replicate the same features.
The research team led by Professor Bart De Strooper at VIB-KU Leuven and the UK Dementia Research Institute (UK DRI) at UCL, created a new model to study Alzheimer’s disease. They implanted both healthy human and mouse neurons into the brains of AD mouse models. Remarkably, only the human neurons, not the mouse neurons, displayed Alzheimer’s features, including tau tangles and significant neuronal cell loss. This highlights the importance of studying human neurons in understanding the mechanisms underlying Alzheimer’s.
The study revealed that necroptosis, a pathway of programmed cell death, was activated in the model, leading to the death of neurons. The researchers also found that the RNA gene MEG3 was strongly increased in human neurons, as seen in Alzheimer’s patients. Interestingly, the presence of MEG3 alone was enough to trigger the pathway of necroptosis in human neurons in a lab setting. The study also showed that by reducing MEG3 and preventing necroptosis, researchers could prevent the death of cells.
This discovery of the involvement of MEG3 and necroptosis in Alzheimer’s provides valuable insights into the mechanisms behind neuronal loss in the disease. Professor De Strooper highlights the potential for developing therapies targeting necroptosis, in addition to traditional approaches focused on amyloid and tau proteins.
Overall, this groundbreaking study unravels the mystery of neuron death in Alzheimer’s and offers hope for future treatments by identifying a potential key player and shedding light on the process of necroptosis.
Sources:
– Medical Research Council [No URL]
– Science [No URL]
